MeSH headings : Animals; Anti-Bacterial Agents / pharmacology; Apoptosis / drug effects; Bacteria / drug effects; Bacteria / genetics; DNA, Bacterial / genetics; DNA, Bacterial / metabolism; Intestinal Mucosa / metabolism; Intestines / microbiology; Intestines / pathology; MAP Kinase Kinase Kinases / genetics; MAP Kinase Kinase Kinases / metabolism; Mice; Mice, Inbred C57BL; Mice, Knockout; Myeloid Differentiation Factor 88 / deficiency; Myeloid Differentiation Factor 88 / genetics; Myeloid Differentiation Factor 88 / metabolism; Necrosis; Paneth Cells / drug effects; Paneth Cells / metabolism; Paneth Cells / pathology; RNA, Messenger / metabolism; Reactive Oxygen Species / metabolism; Real-Time Polymerase Chain Reaction; Receptor-Interacting Protein Serine-Threonine Kinases / genetics; Receptor-Interacting Protein Serine-Threonine Kinases / metabolism; Signal Transduction; Toll-Like Receptors / metabolism; Up-Regulation

TL;DR: It is found that depletion of gut bacteria or myeloid differentiation factor 88 (Myd88), a mediator of bacteria-derived cell signaling, reduced ROS but did not block Paneth cell loss, suggesting that gut bacteria are the cause of ROS accumulation but bacteria-induced ROS are not the cause. (via Semantic Scholar)