Using a rational approach to isolate CD4+FOXP3+ regulatory T (Treg)-cell-inducing bacterial strains from the human indigenous microbiota may allow for tailored therapeutic manipulation of human immune disorders.
It is shown that a large bowel microbial fermentation product, butyrate, induces the differentiation of colonic Treg cells in mice and ameliorated the development of colitis induced by adoptive transfer of CD4+ CD45RBhi T cells in Rag1−/− mice.
It is proposed that acetate produced by protective bifidobacteria improves intestinal defence mediated by epithelial cells and thereby protects the host against lethal infection.
It is reported that a mammalian protein, M-Sec, induces de novo formation of numerous membrane protrusions extending from the plasma membrane, some of which tether onto adjacent cells and subsequently form TNT-like structures.
It is reported that microbiota-induced Tregs express the nuclear hormone receptor RORγt and differentiate along a pathway that also leads to TH17 cells, and acts as a key factor in balancing immune responses at mucosal surfaces.
GP2 is a previously unrecognized transcytotic receptor on M cells for type-I-piliated bacteria and is a prerequisite for the mucosal immune response to these bacteria, which could provide a new target for the development of M-cell-targeted mucosal vaccines.
A novel subset of natural killer T cells that expresses the interleukin 17 receptor B for IL-25 and is essential for the induction of AHR is identified, suggesting that IL-17RB+ CD4+ NKT cells play a crucial role in the pathogenesis of asthma.
The different roles of gut microbiome activity and their metabolites in regulating distinct host physiology and the molecular mechanisms by which gut metabolites cause physiological homeostasis via regulating specific host signaling pathways are described.
It is concluded that differentiated human colon epithelium expresses LL-37/hCAP18 as part of its repertoire of innate defense molecules and that the distribution and regulated expression of LL- 37/h CAP18 in the colon differs markedly from that of other enteric antimicrobial peptides, such as defensins.
Data indicate that H. pylori up-regulates production of LL-37/hCAP18 by gastric epithelium and suggest this cathelicidin contributes to determining the balance between host mucosal defense and H.pylori survival mechanisms that govern chronic infection with this gastric pathogen.