Fig. 2

The interplay between the innate immune system and the gut microbiota in GI tract. Some mechanisms utilized by the gut microbiota to interact with the host innate immune system in GI tract are described above. The interplay between the gut and its microbiota is complex. The secretion of AMPs could be affected by A.muciniphila. PRRs are strongly affected by the presence of the gut microbiota. Microbiota-derived TLR and NOD ligands act directly on intestinal immunocytes and can activate inflammatory genes. Bacteroides fragilis stimulates the downstream PI3K pathway and activates the transcription of anti-inflammatory genes by co-operating TLR1/TLR2 heterodimer and Dectin-1. NLRs function to activate inflammatory caspases and cytokines to compost optimal microbiota and maintain intestinal homeostasis. Microbial metabolites taurine, histamine, and spermine have been identified to regulate the activation of NLRP6 inflammasome as well as the induction of downstream epithelial IL-18 and AMPs secretion. Innate immune cells, including macrophages, DCs, and NK cells, interact heavily with the gut microbiota. OMVs derived from Bacteroides elicit IL-10 production by DCs, as well as enhance the phagocytic functions of macrophages triggered by the bacteria themselves. The expression of the transcription factor RORγt and IL-22 of intestinal NK cells is conditioned by the commensal microbiota