Host strategy for the gut-microbe mutualism.

다국어 초록 (Multilingual Abstract)

In Drosophila gut, recent studies in our laboratory highlight the importance of intestinal epithelium in mediating host antimicrobial defense through the production of microbicidal reactive oxygen species(ROS) and antimicrobial peptides(AMPs)(Jang et al 2006 Dev. Cell; Ha et al 2005 Dev. Cell; Ha et al 2005 Science; Ryu et al 2006 EMBO J.; Ryu et al 2004 Mol. Cell. Biol.). During most gut-pathogen interaction, intestinal redox homeostasis, via the infection-induced de novo generation of ROS by dual oxidase(Duox) and their elimination by immune-regulated catalase(IRC), is critical in the host survival. The direct contact between gut epithelia and ingested pathogens also activates the immune deficiency(IMD) pathway and subsequent nuclear localization of p105-like NF-ĸB, Relish, for the de novo synthesis of diverse inflammatory effectors including AMPs and anti-inflammatory enzymes including peptidoglycan recognition protein(PGRP)-SC and -LB. The intestinal NF-ĸB/AMP system acts as an essential "fail-safe" system complementary to the ROS-dependent gut immunity, during gut infection with ROS-resistant pathogens. Although the nature of gut immunity is fairly well-documented, the molecular regulatory mechanism of gut immunity is poorly known. In this seminar, we will provide evidences about the bi-directional gut-microbe signaling exchange within the context of microbe-rich hostile environment, which is necessary to avoid excessive inflammation and to maintain gut homeostasis.