Redox signaling mediates symbiosis between the gut microbiota and the intestine.

The microbiota that populates the intestinal tract affects many physiological processes, such as cell proliferation, epithelial barrier function, and immune responses. However, the molecular mechanisms by which the microbiota influences these events remain unknown. It was recently reported by our research group that specific taxa of intestinal bacteria induce the rapid and transient enzymatic production of reactive oxygen species (ROS) within enterocytes. Whereas NADPH oxidase 2 (Nox2) catalyzed ROS generation in response to microbial perception by bone marrow-derived phagocytes is well-studied, the function of ROS generated by Nox1 in enterocytes in response to microbial signals is not fully understood. It is established that ROS can act as signaling molecules in diverse transduction pathways by the rapid and transient oxidation of oxidant-sensitive thiol groups harbored within sensor regulatory proteins. Because commensal-bacterial-stimulated ROS generation in enterocytes has been shown to induce a wide range of physiological processes, in our recent manuscript, we proposed a paradigm wherein the influence of the microbiota on intestinal physiology is mediated in part by redox-dependant signaling.