Salmonella enterica serovar Typhimurium periplasmic superoxide dismutases SodCI and SodCII are required for protection against the phagocyte oxidative burst.
Vitamin D(3) (1,25-dihydroxycholecalciferol) induced the phagocyte oxidative burst and intracellular killing of Salmonella enterica serovar Typhimurium in a phosphatidylinositol 3-kinase-dependent manner. The antimicrobial effect was more pronounced for Salmonella SodCI and SodCII mutants, confirming the role of the phagocyte oxidase in the vitamin D(3) effect. The results for an in vitro system with human THP-1 cells correlate with in vivo virulence data for mice and show that both the SodCI and SodCII enzymes are required to protect against the oxidative burst.
Department of Medicine, Division of Infectious Diseases, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
Laura M
LM
Sly
Donald G
DG
Guiney
Neil E
NE
Reiner
D000818:Animals; D002460:Cell Line; D002762:Cholecalciferol / Q000494:pharmacology; D005798:Genes, Bacterial; D006801:Humans; D066298:In Vitro Techniques; D007527:Isoenzymes / Q000235:genetics / Q000378:metabolism; D051379:Mice; D009154:Mutation; D010586:Phagocytes / Q000187:drug effects / Q000378:metabolism* / Q000382:microbiology*; D016897:Respiratory Burst; D012486:Salmonella typhimurium / Q000187:drug effects / Q000201:enzymology* / Q000235:genetics / Q000472:pathogenicity; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism*
D007527:Isoenzymes; D002762:Cholecalciferol; D013482:Superoxide Dismutase