title: Prior Helicobacter pylori infection ameliorates Salmonella typhimurium-induced colitis: mucosal crosstalk between stomach and distal intestine.
abstract: BACKGROUND
  Helicobacter pylori infection is associated with a lower risk of chronic autoimmune diseases including inflammatory bowel disease (IBD). H.pylori modulates the gastric immune response, decreasing the local inflammatory response to itself. In mice, chronic Salmonellatyphimurium infection induces colitis similar to Crohn's disease, characterized by inflammation, which progresses toward fibrosis. The aim of this study was to determine whether prior H. pylori infection acts at a distance to modulate the immune response of S.typhimurium-induced colitis.
  
  
  METHODS
  Mice were infected with the mouse-adapted strain of H. pylori (SS1), followed by infection with S.typhimurium. The effect of H. pylori on colitis was determined by gross pathology, histopathology, cytokine response, and development of fibrosis in the cecum. Gastritis and systemic immune response was measured in response to infection.
  
  
  RESULTS
  H.pylori suppresses the Th17 response to S.typhimurium infection in the mouse cecum, but does not alter the Th2 or T-regulatory response or the development of fibrosis. H. pylori infection induces IL-10 in the mesenteric lymph nodes, suggesting an extragastric mechanism for immunomodulation. H. pylori / S.typhimurium coinfection decreases inflammation in both the cecum and the stomach.
  
  
  CONCLUSIONS
  This study demonstrates a potential mechanism for the negative association between H. pylori and IBD in humans. H. pylori represses the lower gastrointestinal tract Th17 response to bacterially induced colitis via extragastric immunomodulatory effects, illustrating immunological crosstalk between the upper and lower gastrointestinal tract.
authors.affiliation: Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Michigan Hospitals, Ann Arbor, Michigan 48109, USA. Phiggins@umich.edu.
authors.forename: Peter D R
authors.initials: PD
authors.lastname: Higgins
authors.forename: Laura A
authors.initials: LA
authors.lastname: Johnson
authors.forename: Jay
authors.initials: J
authors.lastname: Luther
authors.forename: Min
authors.initials: M
authors.lastname: Zhang
authors.forename: Kay L
authors.initials: KL
authors.lastname: Sauder
authors.forename: Luz P
authors.initials: LP
authors.lastname: Blanco
authors.forename: John Y
authors.initials: JY
authors.lastname: Kao
mesh_terms: D000818:Animals; D002432:Cecum / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D003092:Colitis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D003106:Colon / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D003429:Cross Reactions / Q000276:immunology; D005260:Female; D016481:Helicobacter Infections / Q000276:immunology*; D016480:Helicobacter pylori / Q000276:immunology; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000276:immunology; D016753:Interleukin-10 / Q000276:immunology; D007413:Intestinal Mucosa / Q000276:immunology* / Q000382:microbiology; D051379:Mice; D008810:Mice, Inbred C57BL; D012306:Risk; D012481:Salmonella Infections, Animal / Q000276:immunology*; D012486:Salmonella typhimurium / Q000276:immunology; D058504:Th17 Cells / Q000276:immunology
chemical_list: D016753:Interleukin-10