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Clinical trials
Journal: Nature Medicine
There has been a striking generational increase in life-threatening <em>food</em> <em>allergies</em> in Westernized societies<sup>1,2</sup>. One hypothesis to explain this rising prevalence is that twenty-first century lifestyle practices, including misuse of antibiotics, dietary changes, and higher rates of Caesarean birth and formula feeding have altered <em>intestinal</em> <em>bacterial</em> communities; early-life alterations may be particularly detrimental<sup>3,4</sup>. To better understand how commensal <em>bacteria</em> regulate <em>food</em> <em>allergy</em> in humans, we colonized germ-free mice with feces from <em>healthy</em> or cow's milk allergic (CMA) <em>infants</em><sup>5</sup>. We found that germ-free mice colonized with <em>bacteria</em> from <em>healthy</em>, but not CMA, <em>infants</em> were protected <em>against</em> anaphylactic responses to a cow's milk allergen. Differences in <em>bacterial</em> composition separated the <em>healthy</em> and CMA populations in both the human donors and the colonized mice. <em>Healthy</em> and CMA colonized mice also exhibited unique transcriptome signatures in the ileal epithelium. Correlation of ileal <em>bacteria</em> with genes upregulated in the ileum of <em>healthy</em> or CMA colonized mice identified a clostridial species, Anaerostipes caccae, that protected <em>against</em> an allergic response to <em>food</em>. Our findings demonstrate that <em>intestinal</em> <em>bacteria</em> are critical for regulating allergic responses to dietary antigens and suggest that interventions that modulate <em>bacterial</em> communities may be therapeutically relevant for <em>food</em> <em>allergy</em>.