Early life exposure to microbes plays an important role in immune system development. Germ-free mice, or mice colonized with a low-diversity microbiota, exhibit high serum IgE levels. An increase in microbial richness, providing it occurs in a critical developmental window early in life, leads to inhibition of this hygiene-induced IgE. However, whether this inhibition is dependent solely on certain microbial species, or is an additive effect of microbial richness, remains to be determined. Here we report that mice colonized with a combination of bacterial species with specific characteristics is required to inhibit IgE levels. These defined characteristics include the presence in early life, acetate production and immunogenicity reflected by induction of IgA. Suppression of IgE did not correlate with production of the short chain fatty acids propionate and butyrate, or induction of peripherally induced Tregs in mucosal tissues. Thus, inhibition of IgE induction can be mediated by specific microbes and their associated metabolic pathways and immunogenic properties.

生命早期暴露于微生物在免疫系统发育中起重要作用。无胚小鼠或定植于低多样性微生物群的小鼠表现出较高的血清IgE水平。微生物丰富性的增加（如果它出现在生命早期的关键发育窗口中）会导致这种卫生诱导的IgE受到抑制。但是，这种抑制作用是否仅取决于某些微生物种类，还是微生物丰富度的累加效应，尚待确定。在这里，我们报道需要用具有特定特征的细菌物种组合来定殖的小鼠才能抑制IgE水平。这些确定的特征包括在早期寿命中的存在，乙酸盐的产生和通过IgA的诱导反映的免疫原性。IgE的抑制与粘膜组织中短链脂肪酸的丙酸和丁酸的产生或外周诱导的Treg的诱导均不相关。因此，IgE诱导的抑制作用可以通过特定的微生物及其相关的代谢途径和免疫原性来介导。