Hello to our dedicated community and newcomers alike.
The World Asthma Foundation (WAF) continues its mission to Defeat Asthma by fostering awareness, enhancing education, and promoting research to unravel the complexities of Asthma. We appreciate your interest and partnership as we work towards a world where Asthma is no longer a limiting factor in anyone’s life.
Thank you for being part of our mission. We encourage you to share this information with your healthcare provider and engage in open, productive conversations about your health.
Last week, we explored the intricate interplay between Candida colonization, dysbiosis, inflammation, autoimmune responses, TNF-alpha dysregulation, and comorbidities in the pathogenesis and exacerbation of severe asthma. A critical piece of the puzzle involves a protein secreted by Candida, Candidalysins. These proteins play a significant role in Candida’s virulence and are instrumental in driving the inflammatory response, making them a critical research focus in the context of Asthma.
Candidalysins: A Closer Look
Candida albicans produces a group of cytolytic peptide toxins known as Candidalysins, which disrupt host epithelial barriers, leading to infection and promoting inflammation. Recent research indicates that Candidalysins also exacerbate the severity of asthma by enhancing airway inflammation, making the study of these proteins crucial in understanding and managing severe asthma.
The Inflammatory Role of Candidalysins
Candidalysins are known to damage epithelial cells, triggering an inflammatory response. In the context of asthma, this inflammation can intensify symptoms and exacerbate the severity of the condition. Understanding the specific role of Candidalysins in promoting this inflammation can provide insights into new therapeutic strategies for managing severe asthma.
Candidalysins and Immune Response
Research indicates that Candidalysins play a vital role in triggering a strong immune response, affecting immune cell recruitment and activation. This response is critical in the progression of asthma and can provide potential targets for therapeutic intervention.
Implications for Severe Asthma
The role of Candidalysins in promoting inflammation and triggering immune responses has significant implications for severe asthma. Understanding these implications is crucial for developing more effective management strategies, diagnostic tools, and potential treatments.
Candida in Pulmonary Secretions: A New Study
In addition to the role of Candidalysins in severe asthma, we also want to highlight another recent study that may be relevant to our readers. This study, published in The Open Respiratory Medicine Journal, examined the presence and significance of Candida in pulmonary secretions of patients with bronchitis, mucus plugging, and atelectasis. These are conditions that can affect people with asthma and make breathing difficult. The study found that Candida was often associated with these conditions and may play a role in causing or worsening them. The study also found that patients with Candida in their lungs had a higher risk of respiratory failure and death. The study suggested that treating Candida with antifungal drugs may help some patients improve their lung function and outcomes. However, the study was not conclusive and more research is needed to confirm these findings. This study adds to the growing evidence that Candida may be more than just a harmless colonizer of the lungs and may have important implications for severe asthma. You can read more about this study here.
Research into Candidalysins and their role in severe asthma is ongoing and promising. These cytolytic toxins provide a unique perspective on how Candida can influence the severity and progression of asthma, offering potential new avenues for therapeutic intervention. Another recent study also suggests that Candida may affect lung function and outcomes by causing or worsening bronchitis, mucus plugging, and atelectasis in some patients. These findings indicate that Candida may be more than just a harmless colonizer of the lungs and may have important implications for severe asthma. We’re excited to bring you the latest research on this subject and appreciate your interest and involvement in the Defeat Asthma mission. As we continue to unravel the complexities of Asthma, we hope to empower our readers with knowledge and tools to manage this chronic condition.
The Future of Asthma Research
As we understand more about the interactions between the Candidalysins and our body’s immune response, we will continue to see developments in diagnostic tools and therapies. Unraveling this complex relationship is critical in determining the trajectory of severe asthma and holds the key to future breakthroughs in its management.
Your Role in Our Mission
Our readers are a crucial part of our mission to Defeat Asthma. As we continue to share insights from the latest research, we encourage you to keep informed and to share these findings with your network. Conversations about research like this can help increase public understanding of Asthma, combat stigma, and ultimately contribute to better outcomes for those living with Asthma.
What’s Coming Up Next
In our upcoming posts, we will continue to keep you updated on research into the role of Candidalysins and other pathogenic factors contributing to severe asthma. We will also be delving into lifestyle and environmental factors that affect asthma, and how we can manage these to better control this chronic condition.
Stay Tuned for More
Stay connected with us to get the latest information and insights in the world of Asthma research, management, and advocacy. Subscribe to our newsletter, follow us on social media, and share our resources with your community.
Thank you for being a part of the World Asthma Foundation community. Your involvement, whether as a reader, donor, advocate, or patient, is critical in our fight to Defeat Asthma. We appreciate your commitment and look forward to a future where Asthma no longer limits anyone’s potential.
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.
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.
• 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.
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.
: 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.
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.
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.
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.
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
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.
Common food dye can trigger inflammatory processes, say university researchers
A recent university study funded by the Canadian Institutes of Health Research reflects that long-term consumption of Allura Red food dye can be a potential trigger of inflammatory bowel diseases (IBDs) and potentially other inflammatory diseases processes as well.
Researchers using experimental animal models of IBD found that continual exposure to Allura Red AC harms gut health and promotes inflammation. Researchers using experimental animal models of IBD found that continual exposure to Allura Red AC harms gut health and promotes inflammation.
‘This further understanding will benefit Asthmatics as well,’ said Alan Gray, Director at the World Asthma Foundation . The human gastrointestinal (GI) tract is home to a diverse ecosystem of microbes, known collectively as the microbiota. Among its many roles, the gut microbiota regulates the immune system and protects against harmful pathogens. In fact, the largest part of the immune system, the gut-associated lymphoid tissue, is found in the gut. This network of immune cells and tissues interacts closely with the gut microbiota, influencing inflammation throughout the body including the lungs.
The dye directly disrupts gut barrier function and increases the production of serotonin, a hormone/neurotransmitter found in the gut, which subsequently alters gut microbiota composition leading to increased susceptibility to colitis.
Khan said Allura Red (also called FD&C Red 40 and Food Red 17), is a common ingredient in candies, soft drinks, dairy products and some cereals. The dye is used to add colour and texture to foodstuffs, often to attract children.
The use of synthetic food dyes such as Allura Red has increased significantly over the last several decades, but there has been little earlier study of these dyes’ effects on gut health. Khan and his team published their findings in Nature Communications. Yun Han (Eric) Kwon, who recently completed PhD in Khan’s laboratory, is first author.
“This study demonstrates significant harmful effects of Allura Red on gut health and identifies gut serotonin as a critical factor mediating these effects. These findings have important implication in the prevention and management of gut inflammation,” said Khan, the study’s senior author, a professor of the Department of Pathology and Molecular Medicine and a principal investigator of Farncombe Family Digestive Health Research Institute.
“What we have found is striking and alarming, as this common synthetic food dye is a possible dietary trigger for IBDs. This research is a significant advance in alerting the public on the potential harms of food dyes that we consume daily,” he said.
“The literature suggests that the consumption of Allura Red also affects certain allergies, immune disorders and behavioural problems in children, such as attention deficit hyperactivity disorder.”
Khan said that IBDs are serious chronic inflammatory conditions of the human bowel that affect millions of people worldwide. While their exact causes are still not fully understood, studies have shown that dysregulated immune responses, genetic factors, gut microbiota imbalances, and environmental factors can trigger these conditions.
In recent years there has been significant progress in identifying susceptibility genes and understanding the role of the immune system and host microbiota in the pathogenesis of IBDs. However, similar advances in defining environmental risk factors have lagged, he said.
Khan said that environmental triggers for IBDs include the typical Western diet, which includes processed fats, red and processed meats, sugar and a lack of fibre. He added that the Western diet and processed food also includes large amounts of various additives and dyes.
He added that the study suggests a link between a commonly used food dye and IBDs and warrants further exploration between food dyes and IBDs at experimental, epidemiological and clinical levels.
On the day after World Asthma Day, May 3, 2022, we scanned the globe to find a statement that best sums up the current state of affairs regarding Asthma.
Kudos to tbe U.S National Institute of Environmental Health NIH Statement on World Asthma Day 2022: Toward Improved Asthma Care
Good enough of summary that we want to publish this in its entirety.
Asthma is a serious lung disease; causes chest tightness, wheezing, and coughing; can often be controlled with proper treatment.
Today (May 3, 2022) on World Asthma Day, the National Institutes of Health reaffirms its commitment to biomedical research aimed at preventing the onset of asthma, understanding its underlying causes, and improving the treatment of it. This chronic airway disease, which is characterized by periodic worsening of inflammation that can make it hard to breathe, affects more than 25 million people in the United States, including more than 5 million children. Left untreated, it can be life-threatening.
While scientists have made substantial progress in understanding asthma diagnosis, management, and treatment, therapies to permanently improve breathing for those who suffer from asthma remain elusive. Researchers around the globe are working steadily toward this goal while they seek to better understand and find new ways to manage the disease. They also are continuing research on the underlying causes of disparities in the incidence, care, and prevention of the disease. On the heels of recently updated management and treatment guidelines, researchers anticipate a brighter future for people living with asthma.
Three NIH institutes primarily support and conduct studies on asthma — the National Heart, Lung, and Blood Institute (NHLBI); the National Institute of Allergy and Infectious Diseases (NIAID); and the National Institute of Environmental Health Sciences (NIEHS). Other NIH Institutes and Centers also support and conduct asthma research. NIH scientists and grantees made important advances in understanding, treating, and managing asthma in 2021, which are briefly highlighted as follows:
Asthma and COVID-19
An NHLBI-funded study showed that during the pandemic, asthma attacks, also known as asthma exacerbations, significantly decreased in a large group of children and adolescents, compared to the year before the pandemic. The study also found that telehealth visits among these patients increased dramatically during this time. The study included nearly 4,000 participants aged 5-17 years with a prior diagnosis of asthma. Researchers believe a better understanding of the factors that contributed to these improved outcomes could lead to better asthma control in all children and adolescents, as researchers noted no racial or ethnic differences in health outcomes in this population.
A NIAID-funded study found that asthma does not increase the risk of becoming infected with SARS-CoV-2, the virus that causes COVID-19. This finding came from a six-month household survey of more than 4,000 children and adults conducted between May 2020 and February 2021.
Researchers have known for decades that social determinants of health – conditions like housing, neighborhood, education, income, and healthcare access – can affect the quality of life and asthma-related health outcomes of people living with the disease. NIH scientists are now reporting new advances in understanding the relationship between social determinants of health and asthma.
Black and Hispanic children who live in low-income urban environments in the United States are at particularly high risk for asthma attacks. These children tend to be underrepresented in large trials of new biologic therapies for asthma.
In a recent NIAID-supported clinical trial, the monoclonal antibody mepolizumab decreased asthma attacks by 27% in Black and Hispanic children and adolescents who have a form of severe asthma, are prone to asthma attacks, and live in low-income urban neighborhoods.
In one study, NHLBI-funded investigators demonstrated the importance of housing interventions in improving the health of children with asthma. Poor quality housing is associated with a high level of asthma triggers – including mold, cockroach, mouse, and dust mite allergens – that can pose a health threat to children with asthma. The study showed the feasibility of using targeted interventions – including better pest management, improved ventilation, and moisture reduction – to achieve healthy housing. It showed that such interventions can result in reduced symptoms and hospitalizations due to asthma.
Environmental Exposures and Asthma
Researchers have known for years that asthma can be triggered by substances in the indoor and outdoor environment. New research shows that exposure to some asthma triggers might even occur before birth.
In an NIH-supported study that included grant support from NIEHS and the NHLBI, researchers reported that prenatal exposure to tiny air pollution particles significantly increased the risk for developing asthma in children. The study, which analyzed data from two different study cohorts, focused on a group of mothers and their children, mostly Black or Hispanic, in the Boston area who lived near major roadways with heavy traffic. It found that more than 18% of the children who were exposed to high levels of these so-called ultrafine particles in the womb developed asthma in their preschool years, compared to 7% of children overall in the United States.
An NIEHS clinical study will assess how environmental factors affect disease progression in non-smoking adults who have moderate or severe asthma. The study will focus on the microbiological and genetic factors associated with atopic asthma, also known as allergic asthma, which is triggered by pollen, dust mites, and other allergens. A better understanding of this data might lead to improved treatments for people with this type of asthma, researchers say.
Climate Change and Asthma
Studies have shown that climate change can increase air pollutants such as ground-level ozone, fine particulates, wildfire smoke, and dust, and that these pollutants can exacerbate asthma. Climate change can also affect the production, distribution, and severity of airborne allergens.
NIEHS, NHLBI, and other NIH institutes and centers are leading the NIH Climate Change and Health Initiative. This is a cross-cutting NIH effort to reduce health threats such as asthma that can develop or worsen because of climate change. The initiative will look at these threats across the lifespan and find ways to build health resilience in individuals, communities, and nations around the world. A strategic framework for the Initiative will help guide NIH investments in this area.
An NIEHS-funded study provides examples of how extreme weather events can affect asthma outcomes. For example, as heat waves and droughts become more frequent and prolonged, the risk of large wildfires will likely increase, resulting in poor air quality that makes it more difficult to control asthma. Other climate-change events can lead to longer and more intense pollen seasons, while mold and dampness in homes may cause asthma to develop or worsen preexisting cases.
About the National Institute of Allergy and Infectious Diseases (NIAID): NIAID conducts and supports research—at NIH, throughout the United States, and worldwide—to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID website.
About the National Heart, Lung, and Blood Institute (NHLBI): NHLBI is the global leader in conducting and supporting research in heart, lung, and blood diseases and sleep disorders that advances scientific knowledge, improves public health, and saves lives. For more information, visit www.nhlbi.nih.gov. For additional information about NHLBI’s asthma resources, visit https://www.nhlbi.nih.gov/BreatheBetter.
About the National Institute of Environmental Health Sciences (NIEHS): NIEHS supports research to understand the effects of the environment on human health and is part of the National Institutes of Health. For more information on NIEHS or environmental health topics, visit
About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.
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
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
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
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
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
London, England UK Session “Educating Parents About ‘Seeding And Feeding’ A Baby’s Microbiome”
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.