The hygiene hypothesis is the leading theory for the increasing prevalence of allergies and allergic asthma. Proposed in the 1980s, it states that people exposed to a diversity of microbes through their environment at an early age are protected from developing allergic diseases in adulthood. However, how this “protection” is impacted by changes in microbial exposure across the lifespan is not well understood.
Adult Exposure Differs
To study this, researchers led by Avery August, PhD, Professor of Immunology at Cornell University College of Veterinary Medicine and AAI Vice President, investigated the effect of exposure to broad microbial diversity in adult and newborn mice on the development of allergic airway inflammation.
The study, published in The Journal of Immunology, found that when exposed to an increased diversity of microbes by co-housing with pet store mice, adult specific pathogen-free (SPF) mice developed enhanced lung inflammation and increased signs of allergic airway disease when exposed to house dust mite allergen. These mice had enhanced TH17/neutrophil rich lung inflammation, which is analogous to TH17/neutrophil type asthma, a more severe form of asthma in humans. Adult SPF mice that were not exposed to increased microbial diversity did not show the same effects when exposed to the allergens.
“Our findings suggest that increased microbial exposure may not always confer protection against developing allergic lung diseases, as predicted by the hygiene hypothesis,” said Dr. August.
Early Exposure offers Protection
Researchers also compared mouse pups that were born and housed in the presence of increased microbial diversity to those born and housed in a specific pathogen-free environment. In contrast to adults, neonates exposed to increased microbial diversity did not have enhanced allergic airway inflammation in response to allergens. This supports that the hygiene hypothesis does hold true when diverse microbial exposure occurs from birth.
“We hope this work is integrated into the field’s understanding of the hygiene hypothesis as it should prompt a more nuanced view of the protective effects of exposure to broad microbial diversity on inflammatory diseases that is based on age of exposure,” shared Dr. August.
The researchers plan to build on this work by investigating whether specific classes of microbes are responsible for age-dependent responses and whether this is applicable to other diseases where microbial exposure impacts susceptibility.
