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Helminth infection promotes colonization resistance via type 2 immunity

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Science  29 Apr 2016:
Vol. 352, Issue 6285, pp. 608-612
DOI: 10.1126/science.aaf3229

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Parasitic worms affect gut microbes

Improved hygiene practices in high-income countries may come with an increased risk of developing inflammatory bowel disease (IBD) or other similar disorders. Ramanan et al. show that intestinal helminth infection, caused by parasitic worms, protects IBD-susceptible mice from developing the disease. The infection increases specific protective species and limits other inflammatory members of the microbiota. People from helminth-endemic regions harbored a similar protective microbiota, and their deworming led to an increase in inflammatory Bacteroidales species, similar to what the authors observed in the mice. Thus, a changing microbial environment may shape susceptibility to inflammatory disease.

Science, this issue p. 608

Abstract

Increasing incidence of inflammatory bowel diseases, such as Crohn’s disease, in developed nations is associated with changes to the microbial environment, such as decreased prevalence of helminth colonization and alterations to the gut microbiota. We find that helminth infection protects mice deficient in the Crohn’s disease susceptibility gene Nod2 from intestinal abnormalities by inhibiting colonization by an inflammatory Bacteroides species. Resistance to Bacteroides colonization was dependent on type 2 immunity, which promoted the establishment of a protective microbiota enriched in Clostridiales. Additionally, we show that individuals from helminth-endemic regions harbor a similar protective microbiota and that deworming treatment reduced levels of Clostridiales and increased Bacteroidales. These results support a model of the hygiene hypothesis in which certain individuals are genetically susceptible to the consequences of a changing microbial environment.

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