title: NADPH oxidases contribute to autophagy regulation.
abstract: Reactive oxygen species (ROS) are emerging as regulators of autophagy in various cellular contexts. There are many cellular sources of ROS in eukaryotic cells. In phagocytes, the critical immune cells for host defense, the Nox2 NADPH oxidase generates ROS during phagocytosis and plays a central role in microbial killing. Toll-like receptors (TLRs) are important membrane microbial sensing receptors, which can activate Nox2,(1) and were recently demonstrated to signal autophagy targeting of phagosomes to promote their maturation.(2) Our recent study reveals that Nox2 activity and its generated ROS are key signals that induce TLR-activated autophagy of phagosomes. Our results provide the first evidence that ROS from the Nox2 NADPH oxidase can contribute to regulating autophagy in host defense against bacteria. The association of TLR, Nox2 and autophagy with inflammatory bowel disease (IBD) suggests a significant role of this antibacterial pathway in these diseases.
authors: Cell Biology Program, Hospital for Sick Children, Toronto, ON, CA.
authors: Ju
authors: J
authors: Huang
authors: John H
authors: JH
authors: Brumell
mesh_terms: D000818:Animals; D001343:Autophagy; D004789:Enzyme Activation; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000201:enzymology / Q000473:pathology; D008954:Models, Biological; D019255:NADPH Oxidases / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism; D012486:Salmonella typhimurium / Q000502:physiology
chemical_list: D017382:Reactive Oxygen Species; D019255:NADPH Oxidases