The metabolic pathways encoded by the human gut microbiome constantly interact with host gene products through numerous bioactive molecules 1. Primary bile acids (BAs) are synthesized within hepatocytes and released into the duodenum to facilitate absorption of lipids or fat-soluble vitamins 2. Some BAs (~5%) escape into the colon, where gut commensal bacteria convert them into a variety of intestinal BAs 2 that are important hormones regulating host cholesterol metabolism and energy balance via several nuclear receptors and/or G protein-coupled receptors 3,4. These receptors play pivotal roles in shaping host innate immune responses 1,5. However, the impact of this host-microbe biliary network on the adaptive immune system remains poorly characterized. Here we report that both dietary and microbial factors influence the composition of the gut BA pool and modulate an important population of colonic Foxp3 + regulatory T cells (Tregs) expressing the transcriptional factor RORγ. Genetic abolition of BA metabolic pathways in individual gut symbionts significantly decreases this Treg population. Restoration of the intestinal BA pool increases colonic RORγ + Treg levels and ameliorates host susceptibility to inflammatory colitis via BA nuclear receptors. Thus, a pan-genomic biliary network interaction between hosts and their bacterial symbionts can control host immunologic homeostasis via the resulting metabolites.

Although maternal antibodies protect newborn babies from infection 1,2 , little is known about how protective antibodies are induced without prior pathogen exposure. Here we show that neonatal mice that lack the capacity to produce IgG are protected from infection with the enteric pathogen enterotoxigenic Escherichia coli by maternal natural IgG antibodies against enterotoxigenic E. coli when antibodies are delivered either across the placenta or through breast milk. By challenging pups that were fostered by either maternal antibody-sufficient or antibody-deficient dams, we found that breast-milk-derived IgG was critical for protection against mucosal disease induced by enterotoxigenic E. coli. IgG also provides protection against systemic infection by E. coli. Pups used the neonatal Fc receptor (FcRn) to transfer IgG from milk into serum. The maternal commensal microbiota can induce antibodies that recognize antigens expressed by enterotoxigenic E. coli and other Enterobacteriaceae species. Induction of maternal antibodies against a commensal Pantoea species confers protection against enterotoxigenic E. coli in pups. This role of the microbiota in eliciting protective antibodies to a specific neonatal pathogen represents an important host defence mechanism against infection in neonates. Reprints and permissions information is available at www.nature.com/reprints.

Metastable orthorhombic phase of AgInS2 nanocrystals with various shapes, including particles, rods, and worms, have been obtained to demonstrate a facile and effective one-pot chemical route for the synthesis of high quality I-III-VI2 ternary semiconductor nanocrystals (AgInS2, CuInS2, AgInSe2) with controllable shape and size.