Staphylococcus aureus enterotoxins (intestinal toxins) have been demonstrated to affect airway disease including Asthma in early life according to multiple studies.
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
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 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 I think.
Those effects on recruiting and getting balance in your mean cells in the lung are really important. When you’ve got a bacterium there that is both 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. You can imagine (the outcomes) when an infant is skewed toward producing those kind of immune cells in these tissues, like the lung, and them having those kind of interactions with mast cells.
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