title: Helicobacter pylori-associated gastric ulcer exhibits enhanced mucosal chemokine activity at the ulcer site.
abstract: OBJECTIVE
  Although mucosal alpha- and beta-chemokines are considered to be involved in the pathogenesis of Helicobacter pylori-associated gastritis, little is known how these chemokines are related to the ulcerogenesis in peptic ulcer patients. We examined the levels of interleukin (IL)-8 and macrophage inflammatory protein-1alpha (MIP-1alpha) in organ cultures and the numbers of inflammatory cells infiltrating the lamina propria by using the mucosal tissues obtained from gastric ulcer (GU) patients with and without H. pylori infection.
  
  
  METHODS
  Levels of IL-8 and MIP-1alpha secreted in organ cultures were measured by an enzyme-linked immunosorbent assay. Numbers of myeloperoxidase-positive neutrophils, CD68-positive macrophages, and mononuclear cells were determined in tissue sections.
  
  
  RESULTS
  The mucosal tissues of both the gastric antrum and the ulcer site obtained from patients with H. pylori-positive GU showed significantly higher levels of IL-8 and MIP-1alpha and increased numbers of inflammatory cells compared with the corresponding mucosal tissues from those with H. pylori-negative GU or the antral mucosal tissues from H. pylori-negative controls. When the values were compared between the mucosal tissues from the gastric antrum and those from the ulcer site, the latter group of tissues showed significantly higher levels of IL-8 and MIP-1alpha and increased numbers of neutrophils and macrophages than the former group regardless of its healing process in patients with H. pylori-positive GU.
  
  
  CONCLUSIONS
  Mucosal alpha- and beta-chemokines may be important to the ulcerogenesis in H. pylori-associated GU disease.
authors.affiliation: First Department of Internal Medicine, Nagoya University School of Medicine, Nagoya, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Shimizu
authors.forename: K
authors.initials: K
authors.lastname: Kusugami
authors.forename: K
authors.initials: K
authors.lastname: Ina
authors.forename: A
authors.initials: A
authors.lastname: Imada
authors.forename: Y
authors.initials: Y
authors.lastname: Nishio
authors.forename: T
authors.initials: T
authors.lastname: Hosokawa
authors.forename: M
authors.initials: M
authors.lastname: Ohsuga
authors.forename: M
authors.initials: M
authors.lastname: Shimada
authors.forename: M
authors.initials: M
authors.lastname: Noshiro
authors.forename: H
authors.initials: H
authors.lastname: Kaneko
authors.forename: T
authors.initials: T
authors.lastname: Ando
mesh_terms: D000328:Adult; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D005260:Female; D016481:Helicobacter Infections / Q000276:immunology* / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D016209:Interleukin-8 / Q000032:analysis / Q000276:immunology*; D007413:Intestinal Mucosa / Q000382:microbiology; D019402:Macrophage Inflammatory Proteins / Q000032:analysis / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D013276:Stomach Ulcer / Q000276:immunology / Q000382:microbiology* / Q000473:pathology
chemical_list: D054405:Chemokine CCL3; D054407:Chemokine CCL4; D016209:Interleukin-8; D019402:Macrophage Inflammatory Proteins