May 6, 2025 – The World Asthma Foundation (WAF) is proud to announce a major new initiative on World Asthma Day aimed at transforming how we understand and manage severe asthma — a condition that continues to affect millions and defy conventional treatment.
Titled “Reframing Severe Asthma: From Ro,” this ongoing series will dig deep into the science and patient experience of severe asthma, exploring overlooked contributors and practical, cost-effective strategies for care. This initiative builds on WAF’s continuing collaboration with leading experts, including Dr. David Corry of Baylor College of Medicine, whose pioneering research into airway mycosis is helping redefine what drives severe asthma in many patients.
“We believe the time has come to stop treating symptoms alone and start asking deeper, root cause, questions about what’s really causing severe asthma—and how we can affordably and effectively address them,” said David B. Corry, M.D., Professor of Medicine-Immunology, Allergy, and Rheumatology, Baylor College of Medicine, Houston, TX, US.
But the scope goes well beyond fungi. The series will also examine:
Bacterial influences in asthma, including Streptococcus pseudopneumoniae and airway microbiome disruption
Mast cell activation and its role in chronic inflammation and systemic symptoms
Genetic predisposition (e.g., ADAM33) and airway remodeling
Environmental and chemical sensitivities increasingly reported by severe asthma sufferers
WAF’s Reframing Severe Asthma series will feature:
In-depth interviews and commentary from thought leaders
Patient stories and clinical case insights
Roundtable discussions and virtual events
A final White Paper and Action Plan for clinicians, researchers, and policymakers
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
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.
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.
Asthma Disparities
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
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.
Most monoclonal antibodies increase the risk of anaphylaxis in severe asthma patients, according to a report published in Clinical and Translational Allergy. The study found 4 out of 5 common mAbs were associated with an increased risk of anaphylaxis. Each of the therapies had a different risk profile. One monoclonal antibody – dupilumab – exhibited a very low risk. The patients in this study were mainly young and middle-aged adults.
What You Need to Know
Monoclonal antibodies (mAbs) are a type of medication designed to work on one specific target, in contrast to conventional medications that often affect more than one site within the body. They differ from polyclonal treatments by binding specifically to a single place (an epitope) on their target protein. Monoclonal antibodies are found naturally, produced by cloned B cells called hybridomas.
For those with severe asthma, there are Clinical Safety Issues. Any severe asthmatic who experiences an anaphylactic reaction due to food or insect allergy must be made aware that the use of mAbs may cause an adverse reaction for them.
Severe asthma patients receiving monoclonal antibodies need close monitoring due to increased anaphylaxis risk, the new study found.
The report, published in Clinical and Translational Allergy, found 4 out of 5 common mAbs were associated with a heightened anaphylaxis risk, though the risk varied from therapy to therapy.
Key Takeaways
Monoclonal antibodies work with the immune system.
mAbs target cancer cells, viruses, bacteria, and other pathogens.
They may be beneficial in autoimmune diseases in place of other immunosuppressive agents.
mAbs generally prevent allergic reactions, but for some people, may cause a severe adverse reaction.
Regular doses of antihistamines and/or epinephrine may be used with the monoclonal antibodies.
Common monoclonal antibodies include:
– omalizumab (trade names Xolair and Omeclamox and used for allergies to asthma and insect bites)
– mepolizumab (trade name Nucala, a newer monoclonal antibody. It is used for Severe Persistent Asthma in those who have moderate to severe allergic asthma and do not respond well to conventional treatments.)
What Are Monoclonal Antibodies?
Monoclonal antibodies are secreted proteins that neutralize a pathogen or an undesirable substance. They derive from monocytes and can bind to target the protein which is responsible for activating B-cells during immune response. They function as a tool to modify the progression of disease by slowing down the symptoms of autoimmune reactions.
Monoclonal Antibodies (MAbs) function to eliminate pathogens or unwanted toxins. They may have diagnostic as well as treatment potentials in autoimmune disease-related disorders.
The World Asthma Foundation thanks the six expert researchers for their insight into how normally beneficial Monoclonal Antibodies may cause Anaphylactic reactions in severe asthmatics.
Li L, Wang Z, Cui L, Xu Y, Guan K, and Zhao B. “Anaphylactic risk related to omalizumab, benralizumab, reslizumab, mepolizumab, and dupilumab.” Published online June 3, 2021. doi:10.1002/clt2.12038
Staphylococcus aureus enterotoxins (intestinal toxins) have a demonstrated effect on airway disease including Asthma in early life according to multiple studies. These bacteria are in the gut and on the skin.
To further the WAF misson to improve our understanding of what drives Severe Asthma, the World Asthma Foundation reached out to Rodney Dietert, PhD, for his thoughts on the topic of Asthma and Staphylococcus aureus.
Rodney Dietert, PhD is a Cornell University Professor Emeritus, Health Scientist Head of Translational Science + Education for SEED, and the Author of the Human Super-Organism How the Microbiome is Revolutionizing the Pursuit of a Healthy Life.
This is the third in the series of interviews on the topic of Asthma and Staphylococcus aureus with Rodney Dietert, Phd.
Today We Learn About
* Staphylococcus aureus beyond the nose including the skin and the gut
Video Interview
Bacteria – Staph A and Asthma
World Asthma Foundation: Dr. Dietert, can we talk about Staphylococcus aureus and Asthma beyond the nose?
Rodney Dietert, PhD: There are skin and gut microbiome effects on the Staph A asthma connection as well. It’s not just the nose but the nose is a good starting point.
Staph A, diet consumption, the bacteria that are in place, particularly in the nose, but also to some extent in the gut and even the skin, can determine what’s going to happen later in the risk for conditions like asthma. I think the thing to realize is that that bacteria and early on, that’s when you’re still recruiting cells. Lung maturation is one of the late-maturing systems. The lung and brain are late compared to a lot of other physiological systems. You don’t really fully mature the lung until something like 18 or 20.
Those effects on recruiting and getting balance in your immune cells in the lung are really important. When you’ve got a bacterium there that is producing allergens, it is stimulating a population we didn’t use to know about, called T helper 9. These cells produce a cytokine called Interleukin-9. The important thing to know is that these cells interact exquisitely with mast cells. They actually have T helper 9 cells.
Immune cells have histamine receptors so they’re co-stimulating between these cells and mast cells. Imagine (the outcomes) when an infant is skewed toward producing that kind of immune cells in these tissues, like the lung, and them having that kind of interactions with mast cells.
To further the WAF mission to improve our understanding of what drives Severe Asthma, the World Asthma Foundation reached out to Rodney Dietert, PhD for his thoughts on the topic of Asthma and the bacteria Staphylococcus aureus.
Staphylococcus aureus (S. aureus) is a Gram positive (thick wall) bacterium that is believed to be carried by about one third of the general population and is responsible for common and serious diseases. A growing amount of medical literature suggest that Staphylococcus aureus enterotoxins (intestinal toxins)could affect airway disease including Asthma.
Rodney Dietert, PhD is a Cornell University Professor Emeritus, Health Scientist Head of Translational Science + Education for SEED and the Author of the Human Super-Organism How the Microbiome is Revolutionizing the Pursuit of a Healthy Life
This is the first interview of three on the topic of Staphylococcus aureus with Rodney Dietert, Phd. We learn about:
* Connection between Asthma and bacteria Staph A * Skin, nose and gut Microbiome * Asthma and the immune system
World Asthma Foundation: Dr. Dietert, can you connect Staphylococcus Aureus or Staph A and Chronic Disease including Asthma for us?
Connection between Asthma and Bacteria Staph A: Video
Rodney Dietert PhD. connects Staph A and Asthma (and other chronic diseases)
Rodney Dietert, PhD: Yes, well, it’s very interesting because there’s a lot of research starting to come out on infectious agents and chronic diseases. We used to think that never the two shall meet but in fact, they do in many cases, either by inducing chronic diseases or by exacerbating those conditions.
Staph A, that is gram-positive bacterium, it is serious in terms of potential infections. We have it most often on the skin and in the nose. It can be either carried there or it can be a transient exposure. It also contributes to food poisoning. It’s one of the agents that, if contaminated, food can produce serious GI problems. It has a number of products that it makes including what are called enterotoxins or exotoxins. These can punch holes in cells. They can damage epithelial layers in the gut or in the airways.
They also are very interesting, in the case of Staph A or Staphylococcus aureus because some of these toxins can serve as allergens. They are actually sensitizing agents and that is the unknown, until recently, discovery, that when you’re looking for allergens that may contribute to asthma, you’d better include integral elements of that particular bacterium because that may be your allergen, that you may or may not have tested for.
World Asthma Foundation:Can you explain the interaction between the Microbiome, Staph A and Asthma?
Rodney Dietert, PhD: Well, as with any potential opportunistic pathogen, the status of our microbiome in the body sites that carry it, and that would be where we’re exposed to the environment, so the airways, respiratory system, the skin, the gut, the urogenital tract, the status of that microbiome is incredibly important in terms of whether those pathogens can gain a foothold and then produce an infection. That is absolutely the case with Staph A.
Breaking the skin may give it (an opportunity to infect) , or surgery (as well). You have Staph A, and particularly drug-resistant Staph A, (as) a potential risk with surgeries but, (also) I mentioned food poisoning, breaking the skin. Also, dysbiosis, we call it, or a problem with the microbiome in the nose really can result in (Staph A problems), not just chronic sinusitis or reoccurring infections, but asthma. (The bacterium) can be inducing the condition, (and/or) it can be exacerbating already existing asthma.
Rodney Dietert, PhD: (Staph A) has been identified as one of the major culprits that is in the nose and where it can gain a foothold, (it) can produce some real problems.
World Asthma Foundation:What’s the distinction between infection and colonization in the context of Staph A and Asthma?
Rodney Dietert, PhD: Well, colonization is really where it’s able to attach to the proximity of the epithelium, or maybe directly to the surface. It can then produce its toxins and damage the epithelium and also have a nutrient source and spread. The thing to keep in mind is your friendly bacteria, your microbiota, that are mutualistic bacteria, or commensals they’re also called, the ones that we take as probiotics. Those actually have something like double-digit processes they can use to block pathogens like Staph A. Their being in place and metabolizing, in this case in the nose, is really important.
There is a recent really beautiful study that was published looking at early life and looking at colonization by bacteria in the nose and the prognosis for those children to develop asthma or not and some of the parameters related to that. That is where you can really see that starting to think about Staph A and asthma is critical immediately at birth and in the early few months. That’s where some of these distinctions are made and where, unfortunately, you can set up the immune system for inflammation in the lung.
World Asthma Foundation: You have a background in Immmunotoxicology. Can you define this role?
Rodney Dietert, PhD: Immunotoxicity is basically any environmental or external directed alteration to the immune system, in a negative way, damage to the immune system. That damage can take all kinds of different forms. Now, I have to say in my earlier years as a professor in the era of AIDS, HIV and AIDS, everybody thought, well, it’s all immunosuppression. My mantra has been, I contend that there are very few things that produce (only) pure immunosuppression. Something goes down and usually something else goes up (within the immune system) quite frankly. That part of what goes up is (often) allergy, autoimmunity, and inflammatory disease.
We used to measure, in the earlier days of immunology, we’ll measure things and say, “Wow, the antibody levels are reduced,” or something like that. We weren’t measuring more complex indicators for auto-immunity allergic diseases like asthma and psoriasis, inflammatory conditions. Had we been doing that (measuring the more complex indicators of immune-inflicted chronic diseases), we would see that some things we thought that were either immunosuppressive or not (and deemed safe), were not actually where the excitement (most significant risk) was for damage to the immune system.
The damage (connected to improper immune enhancement/balance) can (lead to) self-inflicted disease produced largely by immune cells (that are) out of control and misregulated. When you’re talking about asthma, that’s where you are. (It) is (that) you have cells and mediators in the lung doing things out of balance that they shouldn’t be doing.
World Asthma Foundation: You advocate and have written extensively about Sustainable Healthcare. In fact, you write about the cost of chronic disease. Can you summarize the findings of the World Economics Council and Harvard study predicting that Chronic Disease will consume 48% of Global GDP by 2030?
Rodney Dietert, PhD: That’s worldwide net worth, and we can’t afford it. If you’re thinking about healthcare being sustainable and being available for people in the future, for our children, for our grandchildren, then we’ve got to do things differently. We should do a better job of preventing chronic diseases like asthma and we certainly should do a better job of managing these (chronic diseases) with the life course in mind.
When a child presents with asthma, the pediatrician quite frankly, in my opinion, should be asking, “What can I do for that child today? What can I do to prevent comorbid diseases 10, 20, 30, 40 years from now?” I think the second part of that we have not yet fully embraced and dealt with.
World Asthma Foundation:What would you like researchers to know about the relationship between Staph A and chronic disease?
Rodney Dietert, PhD: I think they need to realize again that the starting point, birth and the first few months, is the time to do something. (In early life) it is easier (to make the most significant changes) and (those actions taken during early development are) likely to be more permanent (as the infant ages). (Also, there is an opportunity to insulate that child from even some problems, maybe diet or otherwise, later in life that (otherwise) could be a risk factor.
That’s the time to do something. Where you get bigger bang for the buck, is early (in life). Researchers simply need to know to look for infectious agents that are involved with conditions like asthma and to start to realize that their management needs to start and stop with the microbes that are protecting the individual, the friendly microbes or microbiota, and to ensure that that is in balance.
If you’re hoping to nudge the immune system in a more useful way, you’re hoping to control inflammation, it’s my contention that if you don’t correct the microbiome, you’re going to be back in the same boat, on the leakyboat, (the) sinking boat, shortly, with your treatments.
There’s sort of a fingerprint of (the) respiratory microbiome, and particularly in the nose, that reflects asthma existing. There’s the chicken or egg question, which comes first, and what’s a result of (what)? Nevertheless, if you don’t actually address that (the respiratory microbiome which affects both risk of Staph A infection and lung immune status) in any meaningful way, then you’ve got to know that the tendency is there that (it is) going to snap back at some point. It’s going to bite you (with an elevated risk of and/or exacerbation of asthma).
WAF will continue to investigate the link between asthma and bacteria.
