title: Induction of chemokine and cytokine responses by Helicobacter pylori in human stomach explants.
abstract: BACKGROUND
  The cytokine response during the acute phase of Helicobacter pylori infection in humans has not been studied. The aim of this study was therefore to investigate the early cytokine responses against H. pylori using cultured human stomach explants as a model of acute infection.
  
  
  METHODS
  Gastric corpus tissue obtained from 13 adult uninfected and 3 H. pylori-infected patients undergoing gastric surgery due to obesity was used for preparation of mucosal explants. The cultured explants were exposed to different H. pylori strains or antigens, that is, lipopolysaccharides (LPS), urease and heat-shock protein (Hsp) B. The responses of the CXC chemokines interleukin (IL)-8, growth-related oncogene alpha (GROalpha) and interferon-inducible protein (IP) 10 as well as the CC chemokine regulated on activation normal T-cell expressed and secreted (RANTES) were determined by ELISA. In addition, IL-4, IL-6, IL-10, IL-12, interferon gamma (IFNgamma), tumour necrosis factor alpha (TNFalpha) and granulocyte-macropage-colony stimulating factor (GM-CSF) were studied.
  
  
  RESULTS
  In vitro H. pylori infection of the explants preferentially induced responses of the CXC chemokines GROalpha (P < 0.05) and IL-8 (P < 0.05), whereas the CC chemokine response (RANTES) was weak. In addition, the production of IL-6 was increased after H. pylori infection. Stimulation of the explants with different LPS preparations also induced strong GROalpha, IL-8 and IL-6 responses; the GROalpha responses being significantly higher after stimulation with rough than smooth H. pylori LPS (P < 0.05).
  
  
  CONCLUSIONS
  GROalpha, IL-8 and IL-6 are increased early during acute H. pylori infection and may influence the development of gastric disease.
authors.affiliation: Centre for Gastroenterological Research, Dept. of Medical Microbiology and Immunology, Göteborg University, Sweden. catharina.lindholm@microbio.gu.se
authors.forename: C
authors.initials: C
authors.lastname: Lindholm
authors.forename: M
authors.initials: M
authors.lastname: Quiding-Järbrink
authors.forename: H
authors.initials: H
authors.lastname: Lönroth
authors.forename: A M
authors.initials: AM
authors.lastname: Svennerholm
mesh_terms: D000328:Adult; D001706:Biopsy / Q000379:methods; D018946:Chemokine CCL5 / Q000032:analysis; D018925:Chemokines / Q000032:analysis*; D046508:Culture Techniques / Q000379:methods; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D005260:Female; D005753:Gastric Mucosa / Q000737:chemistry*; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000032:analysis*; D016481:Helicobacter Infections / Q000175:diagnosis / Q000276:immunology*; D016480:Helicobacter pylori / Q000276:immunology / Q000502:physiology*; D006801:Humans; D015850:Interleukin-6 / Q000032:analysis / Q000276:immunology; D016209:Interleukin-8 / Q000032:analysis; D007378:Interleukins / Q000032:analysis*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D018121:Receptors, Cytokine / Q000032:analysis
chemical_list: D018946:Chemokine CCL5; D018925:Chemokines; C104577:IP10-Mig receptor; D015850:Interleukin-6; D016209:Interleukin-8; D007378:Interleukins; D008070:Lipopolysaccharides; D018121:Receptors, Cytokine; D016178:Granulocyte-Macrophage Colony-Stimulating Factor