title: Interactions between inducible nitric oxide and other inflammatory mediators during Helicobacter pylori infection.
abstract: BACKGROUND
  Recent studies in both humans and animal models strongly suggest the contribution of the host immune response to Helicobacter pylori-related disease. Inducible nitric oxide synthase has been shown to be up-regulated in the gastric epithelium during H. pylori gastritis, suggesting a role in inflammation.
  
  
  METHODS
  C57BL/6 wild-type and inducible nitric oxide synthase gene knockout mice were infected with H. pylori strain SS1. Expression of macrophage inflammatory protein-2 (MIP-2), interleukin-1 beta (IL-1 beta), Th1 (IL-2 and gamma interferon) and Th2 (IL-4 and IL-10) cytokines, and inducible cyclooxygenase mRNA in mice was determined in mouse gastric tissues and quantified using either competitive reverse transcription-polymerase chain reaction or competitive polymerase chain reaction following reverse transcription.
  
  
  RESULTS
  The Th1 cytokine gamma interferon was only detected in wild-type and inducible nitric oxide synthase gene knockout infected mice, while a Th2 (IL-4) response was not detected. H. pylori induced MIP-2 and IL-1 beta mRNA in mice.
  
  
  CONCLUSIONS
  Because similar levels of inflammatory mediators were noted in both wild-type and nitric oxide synthase gene knockout infected mice, our data suggest that inducible nitric oxide synthase does not influence expression of these inflammatory mediators in the early stages of H. pylori infection in mice.
authors.affiliation: Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093-0640, USA.
authors.forename: Marygorret
authors.initials: M
authors.lastname: Obonyo
authors.forename: Donald G
authors.initials: DG
authors.lastname: Guiney
authors.forename: Joshua
authors.initials: J
authors.lastname: Fierer
authors.forename: Sheri P
authors.initials: SP
authors.lastname: Cole
mesh_terms: D000818:Animals; D054426:Chemokine CXCL2; D018925:Chemokines / Q000096:biosynthesis; D016207:Cytokines / Q000096:biosynthesis* / Q000235:genetics; D005260:Female; D017353:Gene Deletion; D005786:Gene Expression Regulation; D016481:Helicobacter Infections / Q000201:enzymology* / Q000276:immunology*; D016480:Helicobacter pylori; D007371:Interferon-gamma / Q000096:biosynthesis; D007375:Interleukin-1 / Q000096:biosynthesis; D016753:Interleukin-10 / Q000096:biosynthesis; D007376:Interleukin-2 / Q000096:biosynthesis; D015847:Interleukin-4 / Q000096:biosynthesis; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D019001:Nitric Oxide Synthase / Q000235:genetics / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II; D011451:Prostaglandin-Endoperoxide Synthases / Q000096:biosynthesis; D018417:Th1 Cells / Q000378:metabolism; D018418:Th2 Cells / Q000378:metabolism
chemical_list: D054426:Chemokine CXCL2; D018925:Chemokines; C404915:Cxcl2 protein, mouse; D016207:Cytokines; D007375:Interleukin-1; D007376:Interleukin-2; D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; D011451:Prostaglandin-Endoperoxide Synthases