title: A critical role for IL-7R signaling in the development of Helicobacter felis-induced gastritis in mice.
abstract: OBJECTIVE
  Interleukin (IL)-7 is a critical cytokine in the development of T and B cells and is involved in gastrointestinal pathophysiology. The aim of this study was to investigate the involvement of IL-7 receptor (IL-7R) signaling in Helicobacter-induced gastritis.
  
  
  METHODS
  C57BL/6 mice (n = 40) were inoculated with H. felis. Twenty mice were injected intraperitoneally with neutralizing IL-7R antibody (A7R34) every seventh day for 3 months. Histology, serum anti-H. felis antibody, and gene expression of IL-7, IL-7R, and proinflammatory cytokines in the gastric mucosa were evaluated.
  
  
  RESULTS
  Seventeen of 20 (85%) infected mice without A7R34 developed severe atrophic gastritis, whereas there was no gastritis in A7R34-treated infected mice. There was no difference in the serum levels of anti-H. felis antibody between the 2 groups. IL-7, IL-7R, IL-1alpha, tumor necrosis factor alpha, and interferon gamma messenger RNA expressions were up-regulated in control infected mice, whereas only IL-7 messenger RNA was up-regulated in A7R34-treated infected mice. Immunohistochemistry indicated positive cytoplasmic staining of IL-7 in the gastric epithelial cells.
  
  
  CONCLUSIONS
  These data suggest a critical role for IL-7 receptor signaling in the development of Helicobacter-induced gastritis in mice.
authors.affiliation: Department of Gastroenterology and Endoscopic Medicine, Faculty of Medicine, Kyoto University, 54 Shogoin-Kawara-cho, Sakyo, Kyoto, 606-8507 Japan.
authors.forename: M
authors.initials: M
authors.lastname: Ohana
authors.forename: K
authors.initials: K
authors.lastname: Okazaki
authors.forename: C
authors.initials: C
authors.lastname: Oshima
authors.forename: D
authors.initials: D
authors.lastname: Andra's
authors.forename: T
authors.initials: T
authors.lastname: Nishi
authors.forename: K
authors.initials: K
authors.lastname: Uchida
authors.forename: S
authors.initials: S
authors.lastname: Uose
authors.forename: H
authors.initials: H
authors.lastname: Nakase
authors.forename: Y
authors.initials: Y
authors.lastname: Matsushima
authors.forename: T
authors.initials: T
authors.lastname: Chiba
mesh_terms: D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D001835:Body Weight; D005753:Gastric Mucosa / Q000382:microbiology / Q000473:pathology; D005756:Gastritis / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology*; D015870:Gene Expression / Q000276:immunology; D016481:Helicobacter Infections / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D007375:Interleukin-1 / Q000235:genetics / Q000276:immunology; D015851:Interleukin-7 / Q000032:analysis / Q000235:genetics / Q000276:immunology; D008198:Lymph Nodes / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D012333:RNA, Messenger / Q000032:analysis; D020395:Receptors, Interleukin-7 / Q000032:analysis / Q000235:genetics* / Q000276:immunology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000276:immunology*; D013154:Spleen / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology
chemical_list: D000907:Antibodies, Bacterial; D007375:Interleukin-1; D015851:Interleukin-7; D012333:RNA, Messenger; D020395:Receptors, Interleukin-7; D014409:Tumor Necrosis Factor-alpha