Public Release: 

How dusty or dairy farm air protect against allergies

American Association for the Advancement of Science

This news release is available in Japanese.

Regular exposure to bacteria particles and farm dust protects children from allergies because it blunts their inflammatory immune responses, a new mouse study suggests. The study implicates a particular anti-inflammatory enzyme, A20, in this protective effect. While aspects of how allergies develop remain unclear, scientists know they're driven not only by genes but also by environment. Homes with pets, as well as dairy farms - where children breathe dust containing higher doses of fungal particles, cowshed-derived bacteria and the bacterial component endotoxin - defend against allergies, recent studies suggest, yet just how has remained elusive. Now, Martijn J. Schuijs et al. shed light on this mystery. The researchers exposed mice to endotoxin every other day for two weeks. They then presented these mice with allergy-driving house dust mites, which often cause asthma in people, finding that mice that had been regularly exposed to endotoxin did not develop allergic features, while control mice did. Endotoxin exposure appears to have protected the mice by squashing the ability of the animals' lung epithelial cells to generate pro-inflammatory molecules, though this protective effect only worked in the presence of a good copy of the enzyme A20. To confirm that A20 had to be functional for the protective effect to work, the researchers turned to humans, using lung biopsy samples from healthy adults and asthmatics. After regular exposure to endotoxin, healthy human cells generated fewer inflammatory molecules characteristic of allergies than their asthmatic counterparts, in whom A20 levels were also lower. This suggests that farming and other similar environments protect against allergy with this enzyme's help.

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Article #15: "Farm dust and endotoxin protect against allergy through A20 induction in lung epithelial cells," by M.J. Schuijs; M.A. Willart; K. Vergote; K. Deswarte; F.B. Madeira; R. Beyaert; G. van Loo; B.N. Lambrecht; H. Hammad at VIB Inflammation Research Center in Ghent, Belgium; M.J. Schuijs; M.A. Willart; K. Vergote; K. Deswarte; F.B. Madeira; R. Beyaert; G. van Loo; B.N. Lambrecht; H. Hammad at Ghent University in Ghent, Belgium; D. Gras; P. Chanez at INSERM in Marseille, France; D. Gras; P. Chanez at CNRS in Marseille, France; D. Gras; P. Chanez at Aix Marseille University in Marseille, France; M.J. Ege; E. von Mutius at Dr. von Hauner Children's Hospital in Munich, Germany; M.J. Ege; E. von Mutius; F. Bracher at Ludwig-Maximilians-Universität in Munich, Germany; B.N. Lambrecht at Erasmus University Medical Center in Rotterdam, Netherlands.

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