Summary:
In humans, Salmonella enterica serovar Typhimurium (S. Typhimurium) is an important cause of acute gastroenteritis. A critical step in host defense is the generation of reactive oxygen species (ROS) generated from NADPH oxidase. NADPH oxidase has multiple subunits, and mutations in various subunits may contributed to increased susceptibility to infection. Dr. Hai Ning Shi and colleagues, with the assistance of the Genomics and Cell Biology Core, elucidated the importance of the p40phox subunit of NADPH oxidase, demonstrating that mice lacking p40phox are more susceptible to infection with S. Typhimurium, as evidenced by bacterial dissemination to the liver and spleen and development of exacerbated colitis. Functional analysis of macrophages and neutrophils demonstrated that absence of p40phox impaired intracellular ROS production and pathogen killing.
Citation:
p40 phox -Deficient Mice Exhibit Impaired Bacterial Clearance and Enhanced Pro-inflammatory Responses during Salmonella enterica serovar Typhimurium Infection. Li Y, Lv M, Su C, Long S, Zhang W, Conway KL, Li W, Xavier RJ, Shi HN. Front Immunol. 2017 Oct 9;8:1270. doi: 10.3389/fimmu.2017.01270. eCollection 2017. PMID: 29062317
Research Center: Harvard Medical School
Featured NORC Member: Hai Ning Shi, PhD, DVM, Associate Professor of Pediatrics, Massachusetts General Hospital and Harvard Medical School
Center Contribution: Dr. Shi is the Co-Associate Director of the Genomics and Cell Biology Core of the Harvard NORC