A critical role for IL-7R signaling in the development of Helicobacter felis–induced gastritis in mice
Background & Aims: 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...
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Published in: | Gastroenterology (New York, N.Y. 1943) Vol. 121; no. 2; pp. 329 - 336 |
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Main Authors: | , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
New York, NY
Elsevier Inc
01-08-2001
Elsevier |
Subjects: | |
Online Access: | Get full text |
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Summary: | Background & Aims: 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-1α, tumor necrosis factor α, and interferon γ 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.
GASTROENTEROLOGY 2001;121:329-336 |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0016-5085 1528-0012 |
DOI: | 10.1053/gast.2001.26289 |