Millions of severe asthma sufferers are searching for answers, often unaware that airway mycosis—a hidden fungal infection—could be the underlying cause of their chronic respiratory problems. April 5-6, 2025 the World Asthma Foundation is hosting a groundbreaking symposium to explore this critical issue, bringing together experts to shed light on the latest research and treatment strategies.
David B. Corry, MD. Medicine-Immunology, Allergy and Rheumatology, Baylor College of Medicine
The World Asthma Foundation (WAF), in collaboration with Dr. David Corry, a renowned airway mycosis and severe Asthma specialist at Baylor University, is committed to raising awareness about this critical issue and the underlying mechanisms of severe asthma.
To address this knowledge gap and improve patient outcomes, WAF is hosting an online symposium April 5-6, 2025. This blog post lays the groundwork for the event, which will bring together experts to discuss diagnosing and managing airway mycosis in severe Asthma patients.
By fostering collaboration, the symposium aims to unveil the hidden mechanisms of fungal asthma, including the root fungal cause and empower better understanding and treatment options for patients with severe asthma.
Burden of Airway Mycosis
Misdiagnosis and Underdiagnosis: Airway mycosis often mimics other respiratory illnesses and is difficult to diagnose using standard methods, leading to misdiagnosis and delayed treatment. This can worsen symptoms and hinder overall patient outcomes.
Chronic Illness and Suffering: Airway mycosis can cause debilitating symptoms like chronic cough, wheezing, shortness of breath, and chest pain. It significantly reduces patients’ quality of life.
Economic Costs: The economic burden of airway mycosis is substantial. Direct medical costs associated with treatment and hospitalization are high. Additionally, indirect costs due to lost productivity are significant.
Challenges and Gaps in Knowledge
Incomplete Understanding of Causes: Dr. Corry’s research emphasizes the need for further investigation into the exact mechanisms by which fungi contribute to airway diseases. The complex interplay between fungal exposure, immune response, and airway inflammation remains unclear.
Mechanisms of fungal asthma are incompletely understood. Research into how fungi cause asthma has improved with the discovery of virulence factors such as proteases and candidalysin, but this has yet to translate into new therapies. Newer antifungal agents such as peptoids and many others hold great promise for better management of airway mycosis.
Limited Diagnostic Tools: Current diagnostic methods for airway mycosis are often insensitive and lack specificity. This makes timely and accurate diagnosis difficult.
Silos in Treatment Approaches: A fragmented approach often exists in managing airway mycosis. Improved collaboration between pulmonologists, allergists, immunologists, and infectious disease specialists is essential.
The Way Forward
Raising Awareness: Increased awareness among healthcare professionals and the public is crucial for earlier diagnosis and improved treatment outcomes. The WAF symposium directly addresses this need.
Enhanced Diagnostics: Dr. Corry’s work on culturing techniques offers promise for improved fungal detection. Development of more accurate and specific diagnostic tools remains essential for proper diagnosis of airway mycosis. These methods are open source and inexpensive; the main hindrance is regulatory acceptance of new protocols.
Investment in Research: Further research is required to elucidate the underlying causes of airway mycosis, identify new treatment options, and improve patient management strategies. The World Asthma Foundation symposium can serve as a catalyst for such research collaborations.
Conclusion
Airway mycosis poses a significant but under-recognized burden on patients and healthcare systems. By raising awareness, improving diagnostics, fostering collaboration, and investing in research, we can effectively address the challenges of this complex disease. The World Asthma Foundation symposium serves as a springboard for this critical work.
Hello, dear members and subscribers of the World Asthma Foundation! We hope you are doing well and breathing easy. In this post, we are going to share with you some news about our Defeating Asthma initiative and our continuing series on Severe Asthma.
As you may know, the World Asthma Foundation is a community-based non profit that aims to raise awareness, provide education and support, and advocate for better care and treatment for people living with Asthma. We believe that everyone deserves to breathe freely and enjoy life without the burden of Asthma.
One of our main goals is to shed light on the different types of asthma and how they affect people differently. As most of you already know, Asthma is not a one-size-fits-all condition. It has many subtypes or phenotypes and some yet to be discovered that have different causes, triggers, symptoms, and responses to treatment. Understanding your Asthma phenotype can help you and your doctor find the best management plan for you.
That’s why we continue our focus on Severe Asthma, a challenging form of Asthma that affects about 5-10% of people with Asthma and consumes 80 % of the dollars to treat. Severe Asthma is often difficult to control with standard medications and can have a significant impact on your quality of life, health, and well-being.
One of the possible factors that can contribute to severe asthma is fungi. Fungi are microscopic organisms that are found everywhere in the environment. They can grow on plants, animals, soil, water, food, or indoor surfaces. Some fungi can cause infections or allergies in humans, especially in people with weakened immune systems or underlying diseases.
One of the most underdiagnosed and undertreated phenotypes of Severe Asthma: Fungal Asthma.
Fungal Asthma is a type of allergic asthma that is triggered by exposure to certain fungi or molds in the environment.
Fungal Asthma can cause persistent inflammation, mucus production, airway obstruction, and bronchial hyperresponsiveness.
Fungi can Initiate Severe Autoimmune Diseases
Fungal Asthma can be hard to diagnose because it can mimic other types of asthma or respiratory infections. However, it requires specific tests and treatments to improve your symptoms and prevent lung damage.
Fungi can affect the lungs and airways of asthmatics in different ways. They can cause fungal sensitization, which means that the immune system reacts to fungal proteins or components as if they were harmful invaders. This can lead to inflammation, mucus production, bronchoconstriction, and remodeling of the airways. Fungal sensitization can also make the lungs more susceptible to other triggers or infections.
Fungi can also cause fungal infection, which means that they invade and multiply in the lungs or airways. This can cause tissue damage, inflammation, and immune activation. Fungal infection can also complicate or mimic other lung diseases, such as tuberculosis or pneumonia.
Fungal sensitization or infection can occur with different types of fungi, such as Alternaria, Aspergillus, Cladosporium, or Penicillium. However, one of the most common and serious forms of fungal involvement in severe asthma is allergic bronchopulmonary aspergillosis (ABPA). ABPA is a condition where the immune system overreacts to Aspergillus species, which are ubiquitous molds that can grow on decaying organic matter or in moist environments. ABPA can cause severe asthma symptoms, lung damage, bronchiectasis (widening and scarring of the airways), and pulmonary fibrosis (hardening and scarring of the lung tissue).
How do you know if you have fungal sensitization or infection in your lungs or airways? Unfortunately, there is no simple or definitive test for this. The diagnosis of fungal sensitization or infection depends on a combination of clinical and immunological criteria, such as:
• History of exposure to fungi or symptoms suggestive of fungal involvement
• Skin testing with antigens derived from fungi or measurement of specific IgE levels in the blood
• Chest imaging (such as X-ray or CT scan) showing signs of lung damage or infection
• Sputum culture or analysis showing the presence of fungi or fungal components
• Bronchoscopy (a procedure where a thin tube with a camera is inserted into the airways) showing signs of inflammation or infection
• Biopsy (a procedure where a small sample of tissue is taken from the lungs) showing signs of inflammation or infection
The treatment of fungal sensitization or infection in severe asthma depends on the type and severity of the condition. The general goals of treatment are to:
• Reduce the exposure to fungi or eliminate them from the environment
• Control the asthma symptoms and prevent exacerbations
• Reduce the inflammation and damage in the lungs and airways
• Eradicate the fungal infection or reduce its load
The treatment options may include:
• Asthma medications (such as bronchodilators, corticosteroids, leukotriene modifiers, biologics, etc.) to relieve the symptoms and prevent exacerbations
• Antifungal medications (such as itraconazole, voriconazole, posaconazole, etc.) to kill or inhibit the growth of fungi
• Immunotherapy (such as allergen-specific immunotherapy or omalizumab) to reduce the immune response to fungi
• Surgery (such as lobectomy or pneumonectomy) to remove severely damaged parts of the lungs
The effectiveness and safety of these treatments may vary depending on the individual case and response. Therefore, it is important to consult with your doctor before starting any treatment and follow their instructions carefully.
How can you prevent fungal sensitization or infection in your lungs or airways? There are some measures that you can take to reduce your exposure to fungi or their effects on your health, such as:
• Avoid or minimize contact with sources of fungi, such as compost, hay, soil, plants, animals, moldy food, or damp places
• Use a mask, gloves, and protective clothing when handling or working with materials that may contain fungi
• Clean and dry your home regularly and remove any visible mold or mildew
• Use a dehumidifier or air conditioner to reduce the humidity and temperature in your home
• Use a high-efficiency particulate air (HEPA) filter or vacuum cleaner to remove airborne fungi or dust from your home
• Avoid smoking or exposure to secondhand smoke, as it can damage your lungs and increase your risk of infection
• Take your asthma medications as prescribed and monitor your symptoms and lung function regularly
• Seek medical attention promptly if you have any signs or symptoms of fungal sensitization or infection, such as worsening asthma, fever, cough, chest pain, weight loss, or blood in the sputum
Fungi can be a hidden but serious threat for people with severe asthma. However, with proper diagnosis, treatment, and prevention, you can manage your condition and improve your quality of life. If you have any questions or concerns about fungi and severe asthma, talk to your doctor or healthcare provider.
We hope you found this blog post informative and helpful. We would like to thank the author of the paper “A mammalian lung’s immune system minimizes tissue damage by initiating five major sequential phases of defense” for their contribution to the scientific knowledge on this topic. You can read the full paper here: <a href=”https://link.springer.com/article/10.1007/s10238-023-01083-4″>https://link.springer.com/article/10.1007/s10238-023-01083-4</a>
If you want to learn more about the World Asthma Foundation and our efforts to improve the lives of people with asthma, please visit our website: <a href=”https://worldasthmafoundation.org/”>https://worldasthmafoundation.org/</a>
Thank you for reading and stay tuned for more updates from us!
Sources:
How Major Fungal Infections Can Initiate Severe Autoimmune Diseases
Hello and welcome to the World Asthma Foundation blog, where we share the latest news and insights on asthma research and treatment. We are a nonprofit organization dedicated to improving the lives of people with asthma and advancing the science of asthma prevention and cure. Our mission is to raise awareness, educate, and advocate for asthma patients and their families. Our vision is a world free of Asthma.
If you are a Severe Asthmatic, you may have a subtype of asthma called Th17-high asthma. This subtype is characterized by high levels of a molecule called IL-17 in your airways. IL-17 is produced by a type of immune cell called Th17 cell. Th17 cells are normally involved in protecting the body from certain bacteria and fungi. However, in some cases, they can become overactive and produce too much IL-17.
IL-17 is a powerful inflammatory molecule that can worsen your asthma symptoms by:
• Attracting other immune cells, such as neutrophils, to your airways
• Activating tissue cells to secrete mucus and contract airway smooth muscle
• Inducing the production of other inflammatory molecules that cause more damage
• Interfering with the action of steroids, which are the main drugs used to treat asthma
In this blog post, we will explain how IL-17 affects Th17-high asthma and what you can do about it.
How IL-17 affects Th17-high asthma IL-17 plays a key role in driving neutrophilic inflammation in Th17-high asthma. Neutrophils are a type of white blood cell that fight infections and inflammation. However, in Th17-high asthma, they accumulate in the airways and cause damage to the lung tissue. This leads to more severe asthma symptoms and poor response to conventional treatments.
IL-17 can stimulate neutrophils to release harmful substances that can damage the airway lining and cause mucus production, airway narrowing, and airway remodeling.
IL-17 can also make asthma worse by interfering with the action of steroids. Steroids work by suppressing inflammation and reducing the activity of immune cells. However, IL-17 can make some immune cells resistant to steroids, which means that steroids may not work as well for some severe asthmatics.
What you can do about IL-17.
One possible strategy to treat Th17-high asthma is to block IL-17 or its receptor with drugs that can prevent IL-17 from binding to its targets and causing inflammation. Several such drugs have been developed and tested in clinical trials for various inflammatory diseases, such as psoriasis, rheumatoid arthritis, and Crohn’s disease. Some of these drugs have also been tested in Severe Asthmatics who have high levels of IL-17 or neutrophils in their airways.
The results of these trials have been mixed. Some studies have shown that blocking IL-17 can improve lung function, reduce exacerbations, and lower the need for oral steroids in severe asthmatics. Other studies have shown no benefit or even worse outcomes with IL-17 blockers. The reasons for these discrepancies are not clear yet, but may depend on factors such as the type of IL-17 blocker used, the dose and duration of treatment, the characteristics of the patients enrolled, and the endpoints measured.
Therefore, more research is needed to determine whether blocking IL-17 is a viable option for treating severe asthma. We also need to identify which patients are most likely to benefit from this approach and how to monitor their response and safety. We also need to explore other ways to modulate IL-17 production or function in severe asthmatics.
In addition to pharmacological interventions, there are also some lifestyle changes that may help reduce IL-17 levels and improve asthma control. These include:
• Avoiding or reducing exposure to triggers that may activate Th17 cells, such as allergens, infections and pollution
• Eating a balanced diet that contains anti-inflammatory foods, such as fruits, vegetables, nuts and fish
• Exercising regularly, but not too intensely, as moderate exercise can reduce inflammation and improve lung function
• Managing stress levels, as stress can increase inflammation and worsen asthma symptoms
If you have asthma, it is important to consult your doctor regularly and follow their advice on how to manage your condition. Your doctor may perform some tests to determine your asthma subtype and prescribe the best treatment for you.
By understanding how IL-17 affects your asthma and taking steps to reduce its impact, you may be able to breathe easier and enjoy a better quality of life.
We hope that this blog post has given you some insight into the role of IL-17 in severe asthma and the potential challenges and opportunities for targeting it. We will continue to update you on this topic as new findings emerge. In the meantime, if you have any questions or comments, please feel free to contact us or leave a comment below.
Thank you for reading and stay tuned for more blog posts from the World Asthma Foundation. Together we can defeat asthma.
Hello and welcome to the World Asthma Foundation blog, where we share the latest news and information on asthma and related topics. We are a non-profit organization that pursues our mission and vision with a strategy to support the asthma community with educational resources. Our goal is to foster improved outcomes, better doctor-patient relationships, and support joint decision-making. In this way, asthmatics can take charge of their own health.
One of our main areas of focus is Infectious Asthma, which is a term that describes asthma that is triggered or worsened by infections, such as bacteria, viruses, fungi or parasites. Infectious Asthma can affect anyone, but it is more common and severe in children, elderly, immunocompromised or low-income populations. Infectious Asthma can cause more frequent and severe asthma attacks, lung damage, chronic sinusitis, nasal polyps and other complications.
In this article, we will review the current knowledge on one of the most common and potentially harmful triggers of Infectious Asthma: Staphylococcus aureus (S. aureus), a bacterium that can colonize the skin and mucous membranes of humans. S. aureus can produce various toxins, such as staphylococcal enterotoxins (SE), that can act as superantigens and induce an intense immune response in the airways. This can result in increased production of immunoglobulin E (IgE), a type of antibody that mediates allergic reactions, and activation of eosinophils, a type of white blood cell that causes inflammation and tissue damage.
We will also discuss how measuring SE specific IgE (SE-IgE) may help to identify a subgroup of patients with severe asthma who may benefit from specific interventions. Finally, we will provide some key takeaways and recommendations for asthmatics and clinicians.
We hope that this article will be informative and helpful for you. If you have any questions or comments, please feel free to contact us. Thank you for reading.
Summary
In this article, we have reviewed the current knowledge on the role of S. aureus and its enterotoxins in asthma, especially severe asthma. We have summarized the main findings from five recent studies that have investigated the association between SE sensitization and asthma severity, phenotype and inflammation. We have also discussed how measuring SE-IgE may help to phenotype asthmatics and guide treatment decisions. We have provided some key takeaways and recommendations for asthmatics and clinicians. Here are the main points:
• S. aureus and its enterotoxins are important factors in the pathogenesis of asthma, especially severe asthma.
• SE can act as superantigens and induce an intense T cell activation causing local production of polyclonal IgE and resultant eosinophil activation.
• SE can also manipulate the airway mucosal immunology at various levels via other proteins, such as serine-protease-like proteins (Spls) or protein A (SpA), and trigger the release of IL-33, type 2 cytokines, mast cell mediators and eosinophil extracellular traps.
• SE sensitization is associated with increased risk of asthma, more asthma exacerbations, nasal polyps, chronic sinusitis, lower lung function and more intense type-2 inflammation.
• SE sensitization is also linked to allergic poly-sensitization and allergic multimorbidity, such as rhinitis, eczema and food allergy, indicating a possible role of S. aureus in the development of allergic diseases.
• Measuring SE-IgE may help to identify a subgroup of patients with severe asthma who may benefit from specific interventions, such as anti-IgE therapy or antibiotics.
Key Takeaways
• Asthmatics should be aware of the potential role of S. aureus and its enterotoxins in triggering and worsening their asthma symptoms and seek medical advice if they suspect an infection or colonization.
• Asthmatics should avoid contact with S. aureus carriers or sources of contamination, such as contaminated food or water, and practice good hygiene and wound care to prevent infection or colonization.
• Asthmatics should ask their doctors about testing for SE-IgE as part of their asthma phenotyping and management, as it may help to identify a subgroup of patients with severe asthma who may benefit from specific interventions.
• Clinicians should consider measuring SE-IgE in asthmatics, especially those with severe asthma, nasal polyps, chronic sinusitis or allergic multimorbidity, as it may provide valuable information on the underlying mechanisms and phenotypes of asthma and suggest novel therapeutic targets and strategies.
• Clinicians should also monitor the SE-IgE levels and response to treatment in asthmatics who are receiving anti-IgE therapy or antibiotics, as it may help to evaluate the efficacy and safety of these interventions.
Conclusion
Asthma is a complex and heterogeneous disease that can be influenced by various factors, such as allergens, irritants, infections and stress. Among these factors, S. aureus and its enterotoxins have emerged as important triggers and modulators of asthma, especially severe asthma. SE can act as superantigens and induce an intense immune response in the airways, resulting in increased production of IgE and activation of eosinophils. SE can also manipulate the airway mucosal immunology at various levels via other proteins, such as Spls or SpA, and trigger the release of IL-33, type 2 cytokines, mast cell mediators and eosinophil extracellular traps. These mechanisms can lead to more severe asthma phenotype and type-2 inflammation.
SE sensitization is associated with increased risk of asthma, more asthma exacerbations, nasal polyps, chronic sinusitis, lower lung function and more intense type-2 inflammation. SE sensitization is also linked to allergic poly-sensitization and allergic multimorbidity, such as rhinitis, eczema and food allergy, indicating a possible role of S. aureus in the development of allergic diseases. Measuring SE-IgE may help to identify a subgroup of patients with severe asthma who may benefit from specific interventions, such as anti-IgE therapy or antibiotics.
In this article, we have reviewed the current knowledge on the role of S. aureus and its enterotoxins in asthma, especially severe asthma. We have summarized the main findings from five recent studies that have investigated the association between SE sensitization and asthma severity, phenotype and inflammation. We have also discussed how measuring SE-IgE may help to phenotype asthmatics and guide treatment decisions. We have provided some key takeaways and recommendations for asthmatics and clinicians.
We hope that this article has been informative and helpful for you. If you have any questions or comments, please feel free to contact us. Thank you for reading.
References
: Bachert C., Humbert M., Hanania N.A., Zhang N., Holgate S., Buhl R., Bröker B.M. Staphylococcus aureus and its IgE-inducing enterotoxins in asthma: current knowledge. Eur Respir J. 2020;55(4):1901592. doi: 10.1183/13993003.01592-2019.
: Kanemitsu Y., Taniguchi M., Nagano H., Matsumoto T., Kobayashi Y., Itoh H. Specific IgE against Staphylococcus aureus enterotoxins: an independent risk factor for asthma. J Allergy Clin Immunol. 2012;130(2):376–382.e3. doi: 10.1016/j.jaci.2012.04.027.
: Soh J.Y., Lee B.W., Goh A. Staphylococcal enterotoxin specific IgE and asthma: a systematic review and meta-analysis. Pediatr Allergy Immunol. 2013;24(3):270–279.e1-4. doi: 10.1111/pai.12056.
: Schleich F., Brusselle G.G., Louis R., Vandenplas O., Michils A., Van den Brande P., Lefebvre W.A., Pilette C., Gangl M., Cataldo D.D., et al. Asthmatics only sensitized to Staphylococcus aureus enterotoxins have more exacerbations, airflow limitation, and higher levels of sputum IL-5 and IgE. J Allergy Clin Immunol Pract. 2023;11(5):1658–1666.e4. doi: 10.1016/j.jaip.2023.01.021.
: James A., Gyllfors P., Henriksson E.L., Lundahl J., Nilsson G., Alving K., Nordvall L.S., van Hage M., Cardell L.O. Staphylococcus aureus enterotoxin sensitization is associated with allergic poly-sensitization and allergic multimorbidity in adolescents. Clin Exp Allergy. 2015;45(6):1099–1107. doi: 10.1111/cea.12519.
Sidebar: What is Staphylococcus aureus?
Staphylococcus aureus is a type of bacteria that can cause various infections in humans and animals. It is found in the environment and also in the normal flora of the skin and mucous membranes of most healthy individuals. It can colonize the anterior nares (the front part of the nose), the throat, the skin, and the gastrointestinal tract. It is estimated that up to half of all adults are colonized by S. aureus, and approximately 15% of them persistently carry it in their noses.
S. aureus can cause infections when it breaches the skin or mucosal barriers and enters the bloodstream or internal tissues. These infections can range from mild skin infections, such as boils or impetigo, to more serious infections, such as pneumonia, endocarditis, osteomyelitis, septic arthritis, or sepsis. S. aureus can also produce toxins that can cause food poisoning, toxic shock syndrome, or scalded skin syndrome.
S. aureus is a very adaptable and versatile bacterium that can acquire resistance to various antibiotics. The most notorious example is methicillin-resistant S. aureus (MRSA), which is resistant to most beta-lactam antibiotics, such as penicillins and cephalosporins. MRSA can cause infections both in community-acquired and hospital-acquired settings and poses a major public health challenge.
S. aureus is believed to have originated in Central Europe in the mid-19th century and has since evolved and diversified into many different strains or clones. Some of these strains are more virulent or resistant than others and have spread globally through human migration and travel. One of these strains is ST8, which includes the USA300 clone that is responsible for most community-acquired MRSA infections in the United States.
S. aureus is one of the most common and potentially harmful triggers of Infectious Asthma, especially severe asthma. It can produce various toxins, such as staphylococcal enterotoxins (SE), that can act as superantigens and induce an intense immune response in the airways. This can result in increased production of immunoglobulin E (IgE), a type of antibody that mediates allergic reactions, and activation of eosinophils, a type of white blood cell that causes inflammation and tissue damage.
The World Asthma Foundation (WAF). WAF is a nonprofit organization dedicated to improving the lives of people with asthma through education, research, and advocacy. In this blog post, I want to share with you some exciting findings from a recent study on the microbiome and asthma, published by Spanish researchers in the journal Nutrients.
The microbiome is the collection of microorganisms that live in and on our bodies, such as bacteria, fungi, viruses, and parasites. The microbiome plays an important role in our health and immunity, and can also influence our susceptibility and response to various diseases, including asthma.
Asthma is a chronic inflammatory disease of the airways that affects millions of people worldwide. Asthma can be triggered by different factors, such as allergens, infections, pollution, stress, and diet. Asthma can also have different phenotypes (characteristics), such as allergic or non-allergic, eosinophilic or non-eosinophilic, mild or severe.
What is the microbiome and how does it affect asthma?
The study by Valverde-Molina and García-Marcos reviews the current evidence and challenges on the relationship between the microbiome and asthma, specifically how microbial dysbiosis (an imbalance of the microbial communities in the body) can influence the origins, phenotypes, persistence, and severity of asthma.
How different factors can influence the microbiome and asthma
The study explores how different factors, such as diet, environment, genetics, and infections, can affect the microbiome and asthma, and how modulating the microbiome could be a potential strategy for preventing or treating asthma. The study also reviews the different methods and techniques used to study the microbiome and its interactions with the immune system and the respiratory system.
The gut-lung axis: a key connection between the microbiome and asthma
One of the key points of the study is the importance of the gut-lung axis in the origin and persistence of asthma. The gut-lung axis is the concept that describes how the gut and lung microbiomes communicate with each other through various pathways, such as metabolites, cytokines, antibodies, and immune cells. The gut-lung axis can modulate inflammation and allergic responses in both organs.
The study shows that the process of microbial colonization in the first three years of life is fundamental for health, with the first hundred days of life being critical. Different factors are associated with early microbial dysbiosis, such as caesarean delivery, artificial lactation and antibiotic therapy, among others.
How microbial dysbiosis can lead to different asthma phenotypes and severity
Longitudinal cohort studies on gut and airway microbiome in children have found an association between microbial dysbiosis and asthma at later ages of life. A low ?-diversity (the number of different species) and relative abundance of certain commensal gut bacterial genera in the first year of life are associated with the development of asthma. Gut microbial dysbiosis, with a lower abundance of Phylum Firmicutes (a group of bacteria that includes lactobacilli), could be related with increased risk of asthma.
Upper airway microbial dysbiosis, especially early colonization by Moraxella spp. (a type of bacteria that can cause respiratory infections), is associated with recurrent viral infections and the development of asthma. Moreover, the bacteria in the respiratory system produce metabolites (substances produced by metabolism) that may modify the inception of asthma and its progression.
The role of the lung microbiome in asthma development has yet to be fully elucidated. Nevertheless, the most consistent finding in studies on lung microbiome is the increased bacterial load (the number of bacteria) and the predominance of proteobacteria (a group of bacteria that includes Haemophilus spp. and Moraxella catarrhalis), especially in severe asthma.
Candida albicans: a fungal culprit in asthma development and exacerbation
The study also mentions Candida albicans (a type of fungus that can cause infections) as one of the fungal genera that can affect the gut and lung microbiome and asthma. Candida albicans can trigger inflammation and autoimmune responses in the body. Candida albicans can also induce a Th17 response (a type of immune response) in the gut and lungs. Candida albicans can also increase lung bacterial load and exacerbate airway inflammation.
This study is very relevant to our own research and findings on Candida’s role in inflammation and autoimmune response: implications for severe asthma. We published an article on this topic on our website on October 13th 2021 which features findings from Mayo Clinic researchers who examined how intestinal fungal microbiota affects lung resident memory CD4+ T cells (a type of immune cell) in patients with asthma.
How modulating the microbiome could be a promising strategy for asthma prevention and treatment
We think that these studies complement each other well and provide valuable insights into this important and emerging topic. We believe that understanding the microbiome and its impact on asthma is crucial for developing new and effective strategies for prevention, diagnosis, and treatment of this chronic disease.
Hello to our dedicated community and newcomers alike.
At the World Asthma Foundation (WAF), we’re united by a singular, important mission: to Defeat Asthma. Our approach is rooted in fostering awareness, enhancing education, and promoting research that seeks to unravel the complexities of Asthma. As we strive towards a world where Asthma is no longer a limiting factor in anyone’s life, we remain steadfast in bringing you timely, comprehensive, and relevant information.
We’re excited to share our latest blog post with you. This post encapsulates the culmination of the efforts of a variety researchers, clinicians, and organizations worldwide working independently including pioneering work from the Mayo Clinic, to shed light on the pathogenesis and exacerbation of severe asthma.
Mayo Clinic Candida Study
We delve into the compelling evidence pointing towards the intricate interplay between Candida colonization, dysbiosis, inflammation, autoimmune responses, TNF-alpha dysregulation, and comorbidities.
As we unravel these complex relationships, our hope is to equip you, our readers, with knowledge that can empower you in your journey with asthma or help you support someone who is affected.
Let’s continue to learn, share, and work together in our collective fight against Asthma.
Thank you for being a part of our mission. We encourage you to share this information with your healthcare provider.
Establishing a trustworthy and effective relationship with a healthcare provider is crucial to managing your health. It not only ensures that you get the best care but also allows for open and productive conversations about your health.
Introduction
Managing Severe Asthma remains a complex task for many pulmonary practitioners, despite available medication and trigger avoidance strategies. Frequent attacks and poor symptom control often plague patients. Recent investigations, pieced together by the World Asthma Foundation over time have uncovered dozens of notable research groups that have illuminated the complex relationship between Candida colonization, dysbiosis, inflammation, autoimmune response, TNF-alpha dysregulation, and comorbidities in the pathogenesis and exacerbation of Severe Asthma. This amassed knowledge underscores the multifaceted nature of Severe Asthma, bringing to light the critical role of Candida in the disease process.
Recent studies reveal a potential link between Candida colonization, dysbiosis, inflammation, autoimmune response, TNF-alpha dysregulation, and comorbidities in the pathogenesis and exacerbation of Severe Asthma. This article will provide an overview of these linkages, the financial impact on individuals and society, the necessity for improved diagnostic tools and processes, and source the scientific studies supporting these conclusions.
Candida Colonization, Dysbiosis, and Fungal Sensitization
Candida albicans, a common fungal inhabitant of the mouth, gut, and genital tract, can also colonize the respiratory tract. This colonization is often facilitated by dysbiosis, an imbalance in the normal microbial flora, which can be induced by various factors, including the use of antibiotics and changes in the host immune response. Further, fungal sensitization, a process where the immune system produces antibodies (IgE) against fungal allergens, plays a crucial role in the onset and severity of asthma symptoms. Studies from the Mayo Clinic underline the lower alpha-diversity of lung microbiota and higher fungal burdens in Asthma patients, showing a correlation with severity and poor control of Asthma.
Case in Point
A recent study presented at the CHEST Annual Meeting 2021 by researchers from Mayo Clinic and University of California Davis confirmed the association between intestinal fungal dysbiosis and asthma severity in humans, particularly hospital use in the past year. The study found that patients with asthma who had higher intestinal Candida burden were more likely to have severe asthma exacerbations in the previous year, independent of systemic antibiotic and glucocorticoid use. This suggests that intestinal fungal dysbiosis may worsen asthma control and outcomes in humans. The study also showed that intestinal fungal dysbiosis can enhance the severity of allergic asthma in mice by increasing lung resident group 2 innate lymphoid cells (ILC2) populations, which are important mediators of the gut-lung axis effect. The study used a novel technique of flow cytometry to identify and quantify ILC2 in the lungs of mice. These findings highlight the potential role of intestinal fungal dysbiosis and ILC2 in asthma pathogenesis and management.
Role of Antibiotics and Gut-Lung Axis
Studies show that certain antibiotics prescribed for infections, such as Helicobacter pylori, can lead to gut microbiota dysbiosis, promoting Candida colonization. This gut-lung axis, the communication between gut microbiota and lung health, can create an environment conducive to fungal overgrowth and subsequent infection. As such, understanding this interaction can offer valuable insights into asthma management. Research from the Mayo Clinic suggests that antibiotic usage can significantly contribute to these interactions and, consequently, the pathogenesis of Severe Asthma.
Mechanisms of Candida Colonization
Candida albicans utilizes several mechanisms to cross the intestinal epithelial barrier, including adherence to epithelial cells, invasion, and translocation. Each of these steps facilitates Candida’s ability to invade the host’s system and trigger an immune response. Insights from the Mayo Clinic suggest that bacterial-fungal interactions play a key role in these mechanisms and have implications for Candida colonization.
Candida-Induced Inflammation, Autoimmune Response, and TNF-alpha Dysregulation
Once established, Candida colonization can incite inflammation by provoking the immune system to produce pro-inflammatory cytokines, such as TNF-alpha. While TNF-alpha aids in fighting off infections by initiating inflammation, its dysregulation can lead to chronic inflammation and autoimmune diseases, enhancing the severity of asthma. Research from the Mayo Clinic has shown that Candida colonization in the lung induces an immunologic response, leading to more Severe Asthma.
Autoimmune Response, Comorbidities, and Severe Asthma
Recent studies propose that an autoimmune response could be involved in the onset and exacerbation of Severe Asthma, with TNF-alpha dysregulation playing a pivotal role. Comorbidities like rheumatoid arthritis, often seen in conjunction with Severe Asthma, can further complicate disease management and progression.
Burden, Financial Impact, and Comorbidities
Severe Asthma imposes a substantial burden on individuals and society, financially and otherwise. Healthcare costs, productivity loss, and reduced quality of life contribute to this impact. Asthma comorbidities such as autoimmune diseases can affect disease progression and outcomes, underscoring the need for a comprehensive management approach.
The Necessity for Improved Diagnostic Tools
An accurate diagnosis of Candida colonization, inflammation, and autoimmune response in severe asthma is crucial for optimal patient management. There’s a growing need for improved diagnostic methodologies, tools, and processes. Advances in diagnostic techniques, such as bronchoscopy and bronchoalveolar lavage (BAL), can offer valuable insights into Candida colonization and the associated inflammatory and autoimmune processes. The Mayo Clinic’s recent findings, which identify a unique pattern of lower alpha-diversity and higher fungal burden in the lung microbiota of severe asthma patients, further emphasize the need for enhanced diagnostic methods.
Conclusion
Understanding the link between Candida colonization, dysbiosis, inflammation, autoimmune response, TNF-alpha dysregulation, comorbidities, and severe asthma is crucial for medical practitioners dealing with this chronic disease. The significant burden and financial impacts of Severe Asthma on individuals and society underline the urgency for effective management strategies.
Recognizing the influence of comorbidities, such as autoimmune diseases, can guide comprehensive care plans for patients with Severe Asthma. Moreover, enhanced diagnostic tools and processes will aid in early identification and more personalized treatment approaches, ultimately improving patient outcomes.
By integrating this knowledge, medical practitioners can not only better understand the multifaceted nature of Severe Asthma but also enhance its overall management, leading to improved patient care. With ongoing research, we can continue to unravel the complex relationships and mechanisms in asthma pathogenesis, providing new avenues for therapeutic interventions and improved patient outcomes.
Research on the relationship between Candida albicans and Asthma is an important area of study that could lead to better understanding and management of Asthma. In the following sections, we will present a summary of various significant studies on the relationship between Candida Albicans colonization and asthma. We will also cover information on the microbiome of the gut and lungs, wherever applicable.
Additionally, we will provide key takeaways from each study, including relevant details such as the study’s title, authors, and organization affiliation. Finally, we will summarize the collective findings and scientific conclusions related to Candida Albicans colonization, sensitization, and infection in Asthma, and offer resources for you to share with your healthcare provider.
A comprehensive understanding of these aspects promises to shed light on the intricate mechanisms underlying severe asthma, offering new perspectives in our fight against this chronic condition.
Further Study
Name of study: Fungal Dysbiosis and Its Clinical Implications in Severe Asthma Patients Date: 2023 Authors: Allison N. Imamura, Hannah K. Drescher, Mai Sasaki, Daniel J. Peaslee, David S. Crockett, Alexander S. Adams, Marcia L. Wills, Stephen C. Meredith, and Andrew H. Limper Organization: Mayo Clinic, Rochester, MN Summary: This study discusses the fungal dysbiosis in severe asthma patients. It finds that the lower alpha-diversity of lung microbiota and higher fungal burdens correlate with severity and poor control of asthma. The study also discusses the possible role of antibiotic usage and bacterial-fungal interactions in this process. The study concludes that understanding the link between Candida colonization, inflammation, autoimmune response, and Severe Asthma is crucial for better management of this chronic disease.
Study Title: CANDIDA ALBICANS INTESTINAL DYSBIOSIS INCREASES LUNG RESIDENT ILC2 POPULATIONS AND ENHANCES THE SEVERITY OF HDM-INDUCED ALLERGIC ASTHMA IN MICE
• Date: October 17-20, 202
Authors: Amjad Kanj, Theodore Kottom, Kyle Schaefbauer, Andrew Limper, Joseph Skalski
• Organization Affiliation: Mayo Clinic and University of California Davis
Human Anti-fungal Th17 Immunity and Pathology Rely on Cross-Reactivity against Candida albicans. Cell 2019. The authors are Petra Bacher, Thordis Hohnstein, Eva Beerbaum, Marie Röcker, Matthew G. Blango, Svenja Kaufmann, Jobst Röhmel, Patience Eschenhagen, Claudia Grehn, Kathrin Seidel, Volker Rickerts, Laura Lozza, Ulrik Stervbo, Mikalai Nienen, Nina Babel, Julia Milleck, Mario Assenmacher, Oliver A. Cornely, Maren Ziegler, Hilmar Wisplinghoff, Guido Heine, Margitta Worm, Britta Siegmund, Jochen Maul, Petra Creutz, Christoph Tabeling, Christoph Ruwwe-Glösenkamp, Leif E. Sander, Christoph Knosalla, Sascha Brunke, Bernhard Hube, Olaf Kniemeyer, Axel A. Brakhage and Carsten Schwarz. The main objective of the article is to investigate how cross-reactivity against Candida albicans influences human anti-fungal Th17 immunity and pathology. • C. albicans-specific Th17 cells can cross-react with other fungal antigens and gluten peptides in patients with CeD or asthma. • Cross-reactive Th17 cells can cause immune pathology in the gut and lung by producing IL-17A and IL-22 cytokines. Candida and asthma better by showing that Candida can induce a specific type of immune response that can also react to other fungi and allergens that are associated with asthma. The article also suggests that Candida may contribute to the severity and chronicity of asthma by causing inflammation and tissue damage in the lung. mechanisms and consequences of cross-reactivity are complex and need further investigation.
Name of study: Candida auris: Epidemiology, biology, a:Authors:ntifungal resistance, and virulence Date: 2020 Authors: Du, H., Bing, J., Hu, T., Ennis, C. L., Nobile, C. J., & Huang, G. M
Name of study: Candida albicans pathogenicity and epithelial immunity Date: 2014 Abstract Naglik, J. R., Richardson, J. P., & Moyes, D. L. URL:
Name of study: Candida albicans interactions with the host: crossing the intestinal epithelial barrier Date: 2019 Abstract: [Unavailable in given data] Authors: Basmaciyan, L., Bon, F., Paradis, T., Lapaquette, P., & Dalle, F. URL: https://doi.org/10.1080/21688370.2019.1612661
Name of study: ACG Clinical Guideline: Treatment of Helicobacter pylori Infection Date: 2017 Abstract: Authors: Chey WD, Leontiadis GI, Howden CW, Moss SF. URL: https://doi.org/10.1038/ajg.2016.563
Name of study: Asthma is inversely associated with Helicobacter pylori status in an urban population Date: 2008 Abstract: [Unavailable in given data] Authors: Reibman J, Marmor M, Filner J, et al. URL: https://doi.org/10.1371/journal.pone.0004060
Name of resource: H pylori Probiotics: A Comprehensive Overview for Health Practitioners Date: 2020 Abstract: Authors: Ruscio M. URL: https://drruscio.com/h-pylori-probiotics/
Name of resource: Treatment regimens for Helicobacter pylori in adults Date: 2022 Abstract: Authors: Lamont JT.
Name of study: Effects of probiotics on the recurrence of bacterial vaginosis: a review Date: 2014 Abstract: Authors: Homayouni A, Bastani P, Ziyadi S, et al.
Welcome to the World Asthma Foundation blog, where we strive to inform and inspire our readers in support of our mission. Today, we turn our attention to a lesser-known aspect of asthma called T2-Low asthma. While much focus has been placed on T2-High asthma, which includes allergic and non-allergic inflammation, T2-Low asthma has remained in the shadows. This subtype encompasses various forms, such as paucigranulocytic asthma, Type 1 and Type-17 inflammation, and the neutrophilic form, which is particularly common in severe or refractory cases. By exploring the realm of T2-Low asthma, we hope to raise awareness, ignite discussion, and rally the asthma community towards much-needed research and innovation.
Subheading: Unraveling the Complexity of T2-Low Asthma
Understanding T2-Low Asthma:
T2-Low asthma comprises different subtypes, including paucigranulocytic asthma, Type 1 and Type-17 inflammation, and the prevalent neutrophilic form. While T2-Low asthma is generally associated with milder symptoms, it’s important to note that the neutrophilic form can result in severe or refractory cases. By recognizing the complexities of T2-Low asthma, we can gain a deeper understanding of the challenges it poses to patients and researchers alike.
The Need for Research:
Despite its impact on patients, T2-Low asthma has received limited attention in terms of biomarkers and effective treatments. The scarcity of research on T2-Low asthma hinders progress in developing targeted therapies and diagnostic tools. By emphasizing the need for increased research efforts, we can work towards improving the lives of individuals living with T2-Low asthma.
Subheading: Key Takeaways
Key Takeaways:
T2-Low asthma encompasses various subtypes, including paucigranulocytic asthma, Type 1 and Type-17 inflammation, and the neutrophilic form. While T2-Low asthma is generally associated with milder symptoms, the neutrophilic form can result in severe or refractory cases. Limited research has been conducted on T2-Low asthma, leading to a lack of biomarkers and effective treatments. Raising awareness and supporting research on T2-Low asthma is crucial to unlocking innovative solutions and improving outcomes for patients. The World Asthma Foundation is dedicated to addressing the gaps in T2-Low asthma research and advocating for the needs of affected individuals. Conclusion:
As we conclude our exploration of T2-Low asthma, we invite you to take action and support the cause. T2-Low asthma remains an understudied and overlooked frontier in asthma research, leaving many patients without effective treatments or biomarkers. It is our collective responsibility to raise awareness, push for solutions, improve diagnostics, and ultimately strive for a cure. By joining hands with the World Asthma Foundation, we can make a significant impact on the lives of those affected by T2-Low asthma. Together, we can transform the future of asthma care and provide hope for a brighter tomorrow.
Severe asthma is a type of asthma that is difficult to control and can have a significant impact on a person’s daily life. Symptoms of severe asthma can include frequent exacerbations (attacks), high levels of asthma symptoms, and a need for high doses of medication to manage symptoms. Causes of severe asthma can include allergies, exposure to environmental triggers, and genetics. Treatment for severe asthma typically includes a combination of long-term control medications, such as inhaled corticosteroids and bronchodilators, as well as quick-relief medications to be taken during exacerbations. In some cases, additional treatments such as biologic medications or immunomodulators may be needed to manage symptoms.
Types of severe Asthma
There are several subtypes of severe asthma that can be characterized based on specific symptoms and causes. These include:
It’s important to note that some people may have characteristics of more than one subtype of severe asthma. It’s important to work with a healthcare professional to identify your specific subtype of asthma and develop a treatment plan that works for you.
Allergic Asthma
Allergic asthma is a subtype of severe asthma that is caused by an allergic reaction to a specific trigger, such as dust mites, mold, animal dander, pollen, or certain foods. The allergens cause the immune system to overreact and release chemicals, such as histamine, which can lead to inflammation and narrowing of the airways.
Allergic asthma: characterized by an allergic reaction to a specific trigger, such as dust mites, mold, or pet dander.
Non-allergic asthma: characterized by symptoms that are not caused by an allergic reaction, but rather by triggers such as viral infections, cold air, or exercise.
Aspirin-exacerbated respiratory disease (AERD): characterized by severe asthma symptoms that are triggered by the use of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs)
Obesity-related asthma: characterized by asthma symptoms that are made worse by being overweight or obese.
Occupational asthma: characterized by symptoms caused by exposure to specific triggers in the workplace, such as chemicals or dusts.
Bronchial thermoplasty: characterized by symptoms caused by structural changes in the airways, such as thickening of the muscle layers that can make it harder to breathe.
Eosinophilic asthma: characterized by a high number of white blood cells called eosinophils in the airways.
Symptoms of allergic asthma can include:
Shortness of breath
Wheezing
Chest tightness
Coughing, especially at night or early in the morning
Difficulty breathing, especially during physical activity
Rapid breathing
Allergic asthma is diagnosed through a combination of medical history, physical examination, and laboratory tests such as skin prick test or blood test (specific IgE) to determine the specific allergens to which an individual is sensitive.
Treatment for allergic asthma typically includes:
Avoiding exposure to allergens as much as possible
Long-term control medications, such as inhaled corticosteroids and bronchodilators
Quick-relief medications to be taken during exacerbations, such as short-acting bronchodilators
Allergen-specific immunotherapy (allergy shots) to help reduce sensitivity to specific allergens over time.
It’s important to note that many people with allergic asthma also have other allergic conditions, such as hay fever, eczema, or hives. They may have benefit from a comprehensive allergy management plan, including allergy testing and immunotherapy.
Non allergic asthma
Non-allergic asthma is a subtype of severe asthma that is not caused by an allergic reaction, but rather by other triggers such as viral infections, cold air, exercise, stress, or exposure to certain chemicals or pollutants. The exact cause of non-allergic asthma is not known, but it is thought to be related to changes in the airways that make them more sensitive to certain triggers.
Symptoms of non-allergic asthma can include:
Shortness of breath
Wheezing
Chest tightness
Coughing, especially at night or early in the morning
Difficulty breathing, especially during physical activity
Rapid breathing
Non-allergic asthma is diagnosed through a combination of medical history, physical examination, and laboratory tests such as pulmonary function test, to rule out other causes of asthma like infections or structural changes.
Treatment for non-allergic asthma typically includes:
Identifying and avoiding triggers as much as possible
Long-term control medications, such as inhaled corticosteroids and bronchodilators
Quick-relief medications to be taken during exacerbations, such as short-acting bronchodilators
Monitoring of symptoms and lung function regularly
It’s important to note that non-allergic asthma and allergic asthma can have similar symptoms and the distinction between the two subtypes can be difficult. A healthcare professional will work with you to identify the specific triggers of your asthma and create an individualized treatment plan.
Mucus Plugs and Asthma
Mucus plugs, also known as bronchial plugs, can be a complication of asthma. Mucus plugs are clumps of thick, sticky mucus that can block the airways and make it harder to breathe. They can form in the airways of people with asthma as a result of inflammation and increased mucus production in the lungs.
Symptoms of mucus plugs in asthma can include:
Shortness of breath
Wheezing
Chest tightness
Coughing, especially at night or early in the morning
Difficulty breathing, especially during physical activity
Rapid breathing
Wet or gurgling sounds when breathing
Increased mucus production and difficulty clearing mucus from the lungs
Mucus plugs can be caused by a number of factors, including exposure to triggers such as allergens, viral infections, or pollutants, as well as by changes in the airways that make them more sensitive to certain triggers.
Treatment for mucus plugs in asthma typically includes:
If you have asthma and are experiencing symptoms of mucus plugs, it’s important to speak with your healthcare professional to develop an individualized treatment plan. In some cases, additional treatments such as biologic medications or immunomodulators may be needed to manage symptoms.
Wheezing and Severe Asthma
Wheezing is a common symptom of severe asthma, as well as other types of asthma. It is a whistling or whistling sound that can be heard when breathing, especially during exhalation. Wheezing is caused by narrowed or obstructed airways, which can make it harder to breathe.
In severe asthma, wheezing can be a sign of increased inflammation and narrowing of the airways, which can lead to difficulty breathing and increased risk of exacerbations. The increased airflow resistance leads to increased air movement velocity, generating the wheezing sound.
Symptoms of severe asthma can include:
Frequent exacerbations (attacks)
High levels of asthma symptoms, such as shortness of breath, chest tightness, and coughing
A need for high doses of medication to manage symptoms
Increased risk of hospitalization
Difficulty with daily activities and impairment of quality of life
Treatment for severe asthma typically includes a combination of long-term control medications, such as inhaled corticosteroids and bronchodilators, as well as quick-relief medications to be taken during exacerbations. In some cases, additional treatments such as biologic medications or immunomodulators may be needed to manage symptoms.
It’s important to work closely with a healthcare professional to develop an individualized treatment plan for severe asthma. This may include regular monitoring of symptoms and lung function, as well as a plan to manage exacerbations and prevent future attacks.
Identifying and avoiding triggers as much as possible
Long-term control medications, such as inhaled corticosteroids and bronchodilators
Quick-relief medications to be taken during exacerbations, such as short-acting bronchodilators
Chest physical therapy, such as chest clapping and vibration, to help remove mucus from the lungs
Monitoring of symptoms and lung function regularly
On this World Asthma Day, May 3, 2002, The Microbiome First – Pathway to Sustainable Healthcare Summit organization committee invites healthcare professionals, non-communicable disease community leaders, and stakeholders to participate in the inaugural Microbiome First Summit, a virtual event taking place online at MicrobiomeFirst.org this May, 17-19, 2022. FREE to participants.
The event, Microbiome First – Pathway to Sustainable Healthcare Summit, kicks off the inaugural event underwritten and moderated by the
World Asthma Foundation (WAF), which is pleased to announce the
following speakers:
Event Keynote RODNEY DIETERT, PHD Cornell University Professor Emeritus Ithaca, NY, USA
Author of The Human Superorganism. Keynote: “Big Picture View of Our Tiny Microbes”
Researcher Sessions MARIE-CLAIRE ARRIETA, PHD
Associate Professor, departments of Physiology, Pharmacology, and Pediatrics, University of Calgary Calgary AB, CANADA Session:“The early-life mycobiome in immune and metabolic development”
JAEYUN SUNG, PHD
Assistant Professor, Microbiome Program, Center for Individualized Medicine, Mayo Clinic. Rochester, MN, USA Session:“A predictive index for health status using species-level gut microbiome profiling”
KATRINE L. WHITESON, PHD
Assistant Professor, Molecular Biology and Biochemistry School of Biological Sciences
Associate Director, UCI Microbiome Initiative Irvine, CA, USA Session:“High-Fiber, Whole-Food Dietary Intervention Alters the Human Gut Microbiome but Not Fecal Short-Chain Fatty Acids”
LISA AZIZ-ZADEH, PHD
Cognitive neuroscientist; Expert in brain imaging, autism, body cognition
Associate Professor in the USC Chan Division of Occupational Science and Occupational Therapy Los Angeles, CA, USA Session: “Brain-Gut-Microbiome System: Pathways and Implications for Autism Spectrum Disorder”
MARTIN KRIEGEL, MD, PHD
Chief of Rheumatology and Clinical Immunology at University Hospital of Münster
GERMANY
Associate Professor Adjunct of Immunobiology at Yale School of Medicine. Session:“Dietary Resistant Starch Effects on Gut Pathobiont Translocation and Systemic Autoimmunity”
ERICA & JUSTIN SONNENBURG, PHD
Senior research scientist and Associate Professor in the Department of Microbiology and Immunology at the Stanford University School of Medicine. Palo Alto, CA, USA Session:“Gut-microbiota-targeted diets modulate human immune status”
EMMA HAMILTON-WILLIAMS, PHD
Associate Professor
Principal Research Fellow
The University of Queensland Diamantina Institute
Faculty of Medicine
The University of Queensland
Translational Research Institute
Woolloongabba, QLD, AUSTRALIA Session:“Metabolite-based Dietary Supplementation in Human Type 1 Diabetes is associated with Microbiota and Immune modulation”
ANDRES CUBILLOS-RUIZ, PHD
Scientist, Wyss Institute of Harvard University and Institute of Medical Engineering and Science at Massachusetts Institute of Technology Cambridge, MA, USA Session:“Protecting the Gut Microbiota from Antibiotics with Engineered Live Biotherapeutics”
EMERAN A MAYER, MD
Gastroenterologist, Neuroscientist, Distinguished Research Professor
Department of Medicine, UCLA David Geffen School of Medicine
Executive Director, G. Oppenheimer Center for Neurobiology of Stress and Resilience at UCLA
Founding Director, UCLA Brain Gut Microbiome Center. Los Angeles, CA, USA Session: “The Gut–Brain Axis and the Microbiome: Mechanisms and Clinical Implications”
BENOIT CHASSAING, PHD
Principal Investigator, Chassaing Lab
Associate professor, French National Institute of Health and Medical Research. Paris, FRANCE Session:“Ubiquitous food additive and microbiota and intestinal environment”
SEI WON LEE, MD, PHD
Associate Professor
College of Medicine, University of Ulsan
Department of Pulmonary and Critical Care, Asan Medical Center Seoul, KOREA Session: “The Therapeutic Application of Gut-Lung Axis in Chronic Respiratory Disease”
PATRICIA MACCHIAVERNI, PHD
Clinical and translational researcher
Research Fellow, The University of Western Australia Perth, WA, AUSTRALIA
Honorary Research Associate, Telethon Kids Institute. Session: “House Dust Mite Shedding in Human Milk: a Neglected Cause of Allergy Susceptibility?”
LIEKE VAN DEN ELSEN, PHD
Research Fellow, The University of Western Australia, Australia
Honorary Research Associate, Telethon Kids Institute. Perth, WA, AUSTRALIA Session:“Gut Microbiota by Breastfeeding: The Gateway to Allergy Prevention”
PAUL TURNER, PHD
Rachel Carson Professor of Ecology and Evolutionary Biology, Yale University
Microbiology faculty member, Yale School of Medicine. New Haven, CT, USA Session:“New Yale Center to Advance Phage Research, Understanding, Treatments, Training, Education”
ANDRES CUBILLOS- RUIZ, PHD
Scientist, Wyss Institute of Harvard University and Institute of Medical Engineering and Science of Massachusetts Institute of Technology MIT
Boston, MA, USA Session: “Protecting the Gut Microbiota from Antibiotics with Engineered Live Biotherapeutics”
CLAUDIA S. MILLER, MD, MS
Emeritus Professor,Allergy/Immunology and Environmental Health University of Texas San Antonio, TX, USA Session: “Toxicant-Induced Lost of Tolerance for Chemicals, Foods and Drugs: a Global Phenomenon”
Media Supporter Content TONI HARTMAN
PRINCIPAL
Microbiome Courses
London, England UK Session “Educating Parents About ‘Seeding And Feeding’ A Baby’s Microbiome”
Summit Details:
The goal of the Microbiome First – Sustainable Healthcare Summit is to
improve quality of life at reduced cost by addressing the microbiome
first, as recent research shows that all of these non-communicable diseases have a relationship to the microbiome.
