Category: Asthma and Bacteria

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How a Common Bacterium Can Trigger and Worsen Your Asthma

Introduction

Hello and welcome to the World Asthma Foundation blog, where we share the latest news and information on asthma and related topics. We are a non-profit organization that pursues our mission and vision with a strategy to support the asthma community with educational resources. Our goal is to foster improved outcomes, better doctor-patient relationships, and support joint decision-making. In this way, asthmatics can take charge of their own health.

One of our main areas of focus is Infectious Asthma, which is a term that describes asthma that is triggered or worsened by infections, such as bacteria, viruses, fungi or parasites. Infectious Asthma can affect anyone, but it is more common and severe in children, elderly, immunocompromised or low-income populations. Infectious Asthma can cause more frequent and severe asthma attacks, lung damage, chronic sinusitis, nasal polyps and other complications.

In this article, we will review the current knowledge on one of the most common and potentially harmful triggers of Infectious Asthma: Staphylococcus aureus (S. aureus), a bacterium that can colonize the skin and mucous membranes of humans. S. aureus can produce various toxins, such as staphylococcal enterotoxins (SE), that can act as superantigens and induce an intense immune response in the airways. This can result in increased production of immunoglobulin E (IgE), a type of antibody that mediates allergic reactions, and activation of eosinophils, a type of white blood cell that causes inflammation and tissue damage.

We will also discuss how measuring SE specific IgE (SE-IgE) may help to identify a subgroup of patients with severe asthma who may benefit from specific interventions. Finally, we will provide some key takeaways and recommendations for asthmatics and clinicians.

We hope that this article will be informative and helpful for you. If you have any questions or comments, please feel free to contact us. Thank you for reading.

Summary

In this article, we have reviewed the current knowledge on the role of S. aureus and its enterotoxins in asthma, especially severe asthma. We have summarized the main findings from five recent studies that have investigated the association between SE sensitization and asthma severity, phenotype and inflammation. We have also discussed how measuring SE-IgE may help to phenotype asthmatics and guide treatment decisions. We have provided some key takeaways and recommendations for asthmatics and clinicians. Here are the main points:

•  S. aureus and its enterotoxins are important factors in the pathogenesis of asthma, especially severe asthma.

•  SE can act as superantigens and induce an intense T cell activation causing local production of polyclonal IgE and resultant eosinophil activation.

•  SE can also manipulate the airway mucosal immunology at various levels via other proteins, such as serine-protease-like proteins (Spls) or protein A (SpA), and trigger the release of IL-33, type 2 cytokines, mast cell mediators and eosinophil extracellular traps.

•  SE sensitization is associated with increased risk of asthma, more asthma exacerbations, nasal polyps, chronic sinusitis, lower lung function and more intense type-2 inflammation.

•  SE sensitization is also linked to allergic poly-sensitization and allergic multimorbidity, such as rhinitis, eczema and food allergy, indicating a possible role of S. aureus in the development of allergic diseases.

•  Measuring SE-IgE may help to identify a subgroup of patients with severe asthma who may benefit from specific interventions, such as anti-IgE therapy or antibiotics.

Key Takeaways

•  Asthmatics should be aware of the potential role of S. aureus and its enterotoxins in triggering and worsening their asthma symptoms and seek medical advice if they suspect an infection or colonization.

•  Asthmatics should avoid contact with S. aureus carriers or sources of contamination, such as contaminated food or water, and practice good hygiene and wound care to prevent infection or colonization.

•  Asthmatics should ask their doctors about testing for SE-IgE as part of their asthma phenotyping and management, as it may help to identify a subgroup of patients with severe asthma who may benefit from specific interventions.

•  Clinicians should consider measuring SE-IgE in asthmatics, especially those with severe asthma, nasal polyps, chronic sinusitis or allergic multimorbidity, as it may provide valuable information on the underlying mechanisms and phenotypes of asthma and suggest novel therapeutic targets and strategies.

•  Clinicians should also monitor the SE-IgE levels and response to treatment in asthmatics who are receiving anti-IgE therapy or antibiotics, as it may help to evaluate the efficacy and safety of these interventions.

Conclusion

Asthma is a complex and heterogeneous disease that can be influenced by various factors, such as allergens, irritants, infections and stress. Among these factors, S. aureus and its enterotoxins have emerged as important triggers and modulators of asthma, especially severe asthma. SE can act as superantigens and induce an intense immune response in the airways, resulting in increased production of IgE and activation of eosinophils. SE can also manipulate the airway mucosal immunology at various levels via other proteins, such as Spls or SpA, and trigger the release of IL-33, type 2 cytokines, mast cell mediators and eosinophil extracellular traps. These mechanisms can lead to more severe asthma phenotype and type-2 inflammation.

SE sensitization is associated with increased risk of asthma, more asthma exacerbations, nasal polyps, chronic sinusitis, lower lung function and more intense type-2 inflammation. SE sensitization is also linked to allergic poly-sensitization and allergic multimorbidity, such as rhinitis, eczema and food allergy, indicating a possible role of S. aureus in the development of allergic diseases. Measuring SE-IgE may help to identify a subgroup of patients with severe asthma who may benefit from specific interventions, such as anti-IgE therapy or antibiotics.

In this article, we have reviewed the current knowledge on the role of S. aureus and its enterotoxins in asthma, especially severe asthma. We have summarized the main findings from five recent studies that have investigated the association between SE sensitization and asthma severity, phenotype and inflammation. We have also discussed how measuring SE-IgE may help to phenotype asthmatics and guide treatment decisions. We have provided some key takeaways and recommendations for asthmatics and clinicians.

We hope that this article has been informative and helpful for you. If you have any questions or comments, please feel free to contact us. Thank you for reading.

References

: Bachert C., Humbert M., Hanania N.A., Zhang N., Holgate S., Buhl R., Bröker B.M. Staphylococcus aureus and its IgE-inducing enterotoxins in asthma: current knowledge. Eur Respir J. 2020;55(4):1901592. doi: 10.1183/13993003.01592-2019.

: Kanemitsu Y., Taniguchi M., Nagano H., Matsumoto T., Kobayashi Y., Itoh H. Specific IgE against Staphylococcus aureus enterotoxins: an independent risk factor for asthma. J Allergy Clin Immunol. 2012;130(2):376–382.e3. doi: 10.1016/j.jaci.2012.04.027.

: Soh J.Y., Lee B.W., Goh A. Staphylococcal enterotoxin specific IgE and asthma: a systematic review and meta-analysis. Pediatr Allergy Immunol. 2013;24(3):270–279.e1-4. doi: 10.1111/pai.12056.

: Schleich F., Brusselle G.G., Louis R., Vandenplas O., Michils A., Van den Brande P., Lefebvre W.A., Pilette C., Gangl M., Cataldo D.D., et al. Asthmatics only sensitized to Staphylococcus aureus enterotoxins have more exacerbations, airflow limitation, and higher levels of sputum IL-5 and IgE. J Allergy Clin Immunol Pract. 2023;11(5):1658–1666.e4. doi: 10.1016/j.jaip.2023.01.021.

: James A., Gyllfors P., Henriksson E.L., Lundahl J., Nilsson G., Alving K., Nordvall L.S., van Hage M., Cardell L.O. Staphylococcus aureus enterotoxin sensitization is associated with allergic poly-sensitization and allergic multimorbidity in adolescents. Clin Exp Allergy. 2015;45(6):1099–1107. doi: 10.1111/cea.12519.

Sidebar: What is Staphylococcus aureus?

Staphylococcus aureus is a type of bacteria that can cause various infections in humans and animals. It is found in the environment and also in the normal flora of the skin and mucous membranes of most healthy individuals. It can colonize the anterior nares (the front part of the nose), the throat, the skin, and the gastrointestinal tract. It is estimated that up to half of all adults are colonized by S. aureus, and approximately 15% of them persistently carry it in their noses.

S. aureus can cause infections when it breaches the skin or mucosal barriers and enters the bloodstream or internal tissues. These infections can range from mild skin infections, such as boils or impetigo, to more serious infections, such as pneumonia, endocarditis, osteomyelitis, septic arthritis, or sepsis. S. aureus can also produce toxins that can cause food poisoning, toxic shock syndrome, or scalded skin syndrome.

S. aureus is a very adaptable and versatile bacterium that can acquire resistance to various antibiotics. The most notorious example is methicillin-resistant S. aureus (MRSA), which is resistant to most beta-lactam antibiotics, such as penicillins and cephalosporins. MRSA can cause infections both in community-acquired and hospital-acquired settings and poses a major public health challenge.

S. aureus is believed to have originated in Central Europe in the mid-19th century and has since evolved and diversified into many different strains or clones. Some of these strains are more virulent or resistant than others and have spread globally through human migration and travel. One of these strains is ST8, which includes the USA300 clone that is responsible for most community-acquired MRSA infections in the United States.

S. aureus is one of the most common and potentially harmful triggers of Infectious Asthma, especially severe asthma. It can produce various toxins, such as staphylococcal enterotoxins (SE), that can act as superantigens and induce an intense immune response in the airways. This can result in increased production of immunoglobulin E (IgE), a type of antibody that mediates allergic reactions, and activation of eosinophils, a type of white blood cell that causes inflammation and tissue damage.

References

: Staphylococcus aureus Infection – StatPearls – NCBI Bookshelf

: Global Epidemiology and Evolutionary History of Staphylococcus aureus ST45

: Origin, evolution, and global transmission of community-acquired … – PNAS

: Staphylococcus aureus Infections: Epidemiology, Pathophysiology 

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How the microbiome affects asthma: new insights from a Spanish study

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.

You can find our article here: https://worldasthmafoundation.org/candidas-role-in-inflammation-and-autoimmune-response-implications-for-severe-asthma.htm

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.

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A Critical Window In Early Life for Microbiome and Asthma

disruption of the microbiome in the gut and lung. Image by Clker-Free-Vector-Images from Pixabay

It may seem strange, but disruption of the gut and lung microbiomes, (microorganisms found in a specific environment) is deeply rooted in the Asthma conundrum according to a growing number of medical researchers. There is a critical window in early life that affects the life a baby will live.

Disruption of the Microbiome in the Gut and Lung link to Asthma?

Word from the editor: This is part of a series of articles on the Microbiome and Asthma. The World Asthma Foundation, dedicated to Defeating Asthma aims to unpack a variety of issues including the clinical evidence that connects the Microbiome and Asthma while describing the mechanisms of this disease

This disruption referred to as “Dysbiosis” by medical experts is an imbalance between the types of organism present in a person’s natural microflora, especially that of the gut, thought to contribute to a range of conditions of ill health, including asthma.

Quote

Researchers at the Interuniversity Messerli Research Institute, Medical University Vienna and the Center for Pathophysiology, Infectiology and Immunology, Institute of Pathophysiology and Allergy Research, Medical University also located in Vienna, Austria have published:

* What causes dysbiosis?

Dysbiosis of the gut and lung microbiome may lead to increased severity of asthmatic symptoms, including airway inflammation
* Treatment with probiotics can reduce inflammation and improve asthma control
* Gut dysbiosis increases intestinal permeability which allows inflammatory molecules to enter the blood stream – this triggers an immune response that leads to chronic low-grade systemic inflammation
* Probiotic administration reduces levels of proinflammatory cytokines in circulation by increasing production of anti-inflammatory cytokines such as IL-10 and IL-22 from T regulatory cells (Tregs) within the gastrointestinal tract* There are many different types of bacteria found in both the gut and lungs – each has its own set effects on health; some promote immunity while others promote allergy responses or other inflammatory conditions like asthma

Key Findings

  • humans are mostly microbial (in terms of numbers of cells and genes)
  • immune dysfunction and misregulated inflammation are pivotal in the majority of NCDs
  • microbiome status affects early immune education and risk of NCDs
  • microbiome status affects the risk of certain infections.

Critical Window in Early Life

  • The lungs are not sterile, as doctors once thought
  • Disruption in gut and lung microbiomes can lead to asthma
  • Probiotics can reverse dysbiosis and reduce inflammation
  • There is a critical window in early life that points to whole-of-life

What You Need to Know

  1. The gut microbiome is a key player in asthma
  2. Dysbiosis of the gut and lung microbiome may lead to severity of asthma symptoms
  3. Probiotics can reduce inflammation and improve asthma control
  4. Gut dysbiosis allows inflammatory molecules into the bloodstream, triggering immune response
  5. Probiotics reduce inflammation by increasing anti-inflammatory cytokines
  6. Some gut and lung bacteria promote immunity, others promote allergy and inflammation
  7. There is a critical window in early life

disruption of the microbiome in the gut and lung. Image by Clker-Free-Vector-Images from Pixabay
Disruption of the microbiome in the gut and lung. Image by Clker-Free-Vector-Images from Pixabay

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Asthma and Bacteriophages – What We Know Now

What is a Bacteriophage

According to the U.S. National Institute of Health, Bacteriophages (or “phages”) are viruses that can kill or incapacitate specific kinds of bacteria while leaving other bacteria and human cells unharmed. By gathering naturally-occurring phages, or by modifying or engineering phages to display certain properties, researchers hope to create novel anti-bacterial therapeutics. Researchers connect Asthma and Bacteriophages.

Impact on Asthma

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.

Because phages eliminate bacteria by infecting them, rather by generating compounds like antibiotics which kill bacteria, phages can be used to treat antibiotic-resistant infections. In addition, some evidence suggests that combination therapy containing both phages and antibiotics could prevent bacteria from becoming drug resistant.

Although scientists have been aware of phages and their ability to kill bacteria since 1917, the  first U.S.-based clinical trials of phage therapy have only recently begun. Individual U.S. patients have received phage therapy, but only under emergency investigational new drug protocols.  

World Asthma Foundation: Dr. Papadopoulos, what prompted your research into bacteriophages?

Asthma and Bacteriophages Video

Connecting Asthma and Bacteriophages

Dr. Nikolaos Papadopoulos: For many years, we have been working on the viral aspects of allergic diseases and particularly asthma based on the observation that most of the symptoms, especially the exacerbations of asthma, followed the common cold. There has been a link well-established, with lots of papers and lots of studying on the relationship of a particular virus, rhinoviruses with asthma exacerbations. Then there were more observations about associations, about bacterial infections, again in exacerbations.

Virus – Bacteria Interaction

We have discovered that the viral aspect also drives, to some extent, persistence of asthma, which means that viruses induce factors that trigger remodeling. Repeated infections might lead you to persistent asthma. Then we started looking at the interactions between viruses and bacteria. While we were looking at these specific micro-organisms, we realized that, as many other scientists did, we were actually focusing on our own little field without giving much attention to the wider perspective of the ecology of at least the local niche, the nose or the lungs where we have found in the last decade that you do have a growth of microbiome.

Lung Microbiome

In the past, we thought that in the lungs, there was no microbiome, but in fact, we know now that there is. Of course, there is increased interest generally in the microbiome and its disturbance, what we call dysbiosis in every condition. Then when we focus, we look at asthma. Wherever there is a focus on evaluating the microbiome in health and disease, there’s almost always this dysbiosis, this imbalance. We don’t know whether this is something that causes the disease or is a cause of the disease. However, it is very important to understand these characteristics.

Less Antibiotics

For us, it has been very important to place the different organisms and their interaction within a community and try to understand whether it’s possible, instead of trying to kill everything. That’s what we do with antibiotics. Instead of trying to eliminate our enemies, rather try to balance things and see whether we can have a community which is balanced and as considered resilient to external possible enemies. This is when and how we started looking into the meta-genome, and particularly the virion of the respiratory tract. That is how this all started.

World Asthma Foundation: What were the key findings?

Dr. Papadopoulos: Our observations so far, this is something I’ve been looking into more detail. As we expected, it is much more complicated rather than saying that one microorganism goes up and another one goes down. It’s much more about the ecology of the organisms rather than specific microorganisms.

Dynamics Between Microorganisms

I think this is a major understanding, a leap forward in that we shouldn’t think of microorganisms as individual forces that shape our internal microbiome health. It is the dynamic between microorganisms. It’s much more closer to health or disease because as you have one microorganism grow, then you have less resources for the other.

It is a balance, which is dynamic and happens all the time. This is where we got into bacteriophages in particular. This was something we did not expect. Also, it was not on the list of the viruses that we were focusing on because we’re focusing on the typical RNA viruses, the ones that harm, usually, like viral viruses of flu or RSV.

Bacteriophages As Main Player

Then we saw that the main player, one of the main players within the viral communities within the virion were the bacteriophages. In fact, and I think that’s our main finding, we’re the first to suggest is that there is a deficiency of bacteriophages in the upper respiratory tract, at least of children, this is where we have studied it.

Asthma and Bacteriophages 

We are now looking into different communities, different people, different geographies, et cetera, but the observation was repeated in another cohort. We don’t have many bacteriophages in an asthmatic airway. This is associated with looser network of microorganisms and less robust interaction network between the viruses and the bacteria.

Intervention With Phages

These key findings suggest that we might be able to intervene. This is a very good opportunity for intervention because we know that bacteriophages, mostly in most cases, they don’t harm.

They are in balance with the human host because they need to be there. It’s to both our benefits to control the bacterial populations for them not to overexpand. It’s a natural ally.

There is a possibility that we might be able to intervene using bacteriophages, but of course, this is not as straightforward as an antibiotic where you just give something, you kill whatever is susceptible and then it goes away.

We’re talking now about ecological balances. We need to understand exactly what type of bacteriophage you might need, what dose, at what time, et cetera. This is what we are actually doing now.

World Asthma Foundation: Thank you. What would you like asthmatics to know?

Dr. Papadopoulos: Well, we can look at the glass as half-full, as half-empty.

Glass Half Empty

The half-empty part is that for turning bacteriophage or different bacteriophages into therapy, we do need to do lots of things. Not only understand the mechanisms and select the bacteriophages, et cetera, but also, we have to overcome lots of regulatory hurdles because in our Western society, we can’t still use bacteriophages. They are living organisms. In order to standardize a living organism to provide it as medicine, it is really demanding.

Of course, there are all these questions and you’ve seen what happens now with the vaccines, even though most of them are not living organisms, still, it is very complex and we need to be very, very careful when we are exploring it.

Glass Half Full

On the other hand, what we are understanding of the half-full aspect is that by understanding the mechanisms and the dynamics of these microorganisms, we understand why healthy living, why being close to nature, why avoiding lots of pollutants makes us healthier in every aspect. This is also for people who have asthma.

Simple Advice

We know that some very simple and daily advice, like for example, being closer to nature, like eating healthy, for example, and avoiding things that generate pollution and things that generate inflammation is something that does improve their health.

I would suggest that asthmatics, as everybody else, should embrace the idea of a healthy environment and healthy people within this healthy environment.

Asthma and bacteriophages may soon be shown to be a very useful connection.

Bacteriophages research Dr. Nikolaos Papadopoulos reports.
Dr. Nikolaos Papadopoulos reports on bacteriophage research.
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Asthma and Bacteria: Nose to the Toes

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.

See also Dr. Dietert’s interview about the Gut and Lung connection.

Staph A bacteria - Dr. Dietert.

For full story and video follow the link below

Asthma and Bacteria: Nose to the Toes

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Asthma and Bacteria in Early Life

Staphylococcus aureus enterotoxins (intestinal toxins) have been demonstrated to affect airway disease including Asthma in early life according to multiple studies. The study of Asthma and Bacteria in early life is very interesting.

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.

Asthma and Bacteria in Early Life: Staphylococcus Aureus

This is the second interview of three on the topic of Asthma and Staphylococcus aureus with Rodney Dietert, PhD. Today we learn about:

  • Relationship between Asthma and Staphylococcus aureus
  • Multinational studies on the topic of Asthma and Staphylococcus aureus
  • Importance of diet

 

Asthma and Bacteria in Early Life: Staphylococcus Aureus

World Asthma Foundation: Can you talk about the relationship between Staph A and Asthma as a biomarker in early life?

Rodney Dietert, PhD: Yes. There’s a multi-nation study that was done to look at the nasal microbiome in early life. They were measuring that two, four, six, nine months up through to two years and then looked, among their cohorts, at asthma between ages 6 and 18.

Nasal Microbiota Findings

What they found was really striking. They found four major categories of progression of the nasal microbiota as the infant aged. There was one of those groups where Staph A was the most prevalent bacterium or Staphylococcus, and particularly Staph A, that was present. The two-month major (bacterium). It was the main bacterium.

That group that started that way, at two months, had, I think it ranged from age 6 to 18, they were measuring asthma and that microbiome beginning (2 months). That contributed to 45 to 60% of the asthma among all of those children they were evaluating. Just from that one (microbiota) type. That was really an impressive predictor of asthma in later childhood. That suggests you don’t want to see Staph A like that, in a two-month-year-old baby. If you do, you better do something about it.

Staph A

Now, again, that is still an association but we understand what Staph A does to the immune system, because of what it does in terms of producing toxins that actually are allergens or can be allergens, what it does to IgE production. You know if that is really the prevalent nasal bacteria at that age and that is not what you usually see, that’s a problem. Right there, there is a biomarker in my opinion that should be a red flag. We should be looking to do something about that.

Sweet Consumption

There are also studies in early life that show consumption of sweets is a contributing factor to the risk when you’ve got Staph A in there. Some of the children actually seem to have a receptor detection of sweet issue. There’s a cohort that actually can’t tell that they’ve really had what would be considered an overabundance of sweets. They’re a little resistant to detecting it, so they eat more and that actually will propel them to severe asthma later on. That combination of Staph A, and diet even, is very important.

Asthma and Bacteria in Early Life: Staph A
Asthma and Bacteria in Early Life: Staph A, Rodney Dietert PhD

For additional information on Asthma and Staphylococcus aureus and the WAF defeating Asthma Project, visit:

Defeating Asthma Project

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Asthma and Bacteria Link says Study

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.

See also Dr. Dietert’s interview about the Gut and Lung connection.

Rodney Dietert PhD on the topic of Asthma and the bacteria Staphylococcus aureus.

For more information about Dr. Dietert, visit here.