Human gastric epithelium produces IL-4 and IL-4δ2 isoform only upon Helicobacter pylori infectione
Human gastric epithelium produces IL-4 and IL-4δ2 isoform only upon Helicobacter pylori infectione
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DOI:
10.1177/039463200702000417
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发表时间:
2007-10-01
影响因子:
3.5
通讯作者:
D'Elios, M. M.
中科院分区:
文献类型:
--
作者:
Orsini, B.;Vivas, J. R.;D'Elios, M. M.
Recent evidence suggests that interleukin-4 (IL-4) is related to mucosal tolerance by which an injurious immune response is prevented, suppressed or shifted to a non-injurious response. We investigated the expression of IL-4 and its splice variant isoform IL-4 delta 2 in gastric epithelial cells of healthy subjects and gastritis patients infected with Helicobacterpylori (H. pylori) with or without the cag pathogenicity island (cag-PAI). IL-4 and IL-4 delta 2 mRNAs were evaluated in microdissected gastric epithelium and in AGS cell lines co-cultured with H. pylori B128 or SSI strains. IL-4 mRNA was consistently detected in microdissected gastric epithelial cells from healthy subjects. The IL-4 mRNA expression was low in H. pylori-infected patients, and markedly reduced in cag-PAI-positive ones. IL-4 delta 2 mRNA was expressed on gastric epithelium of H. pylori-infected patients, but not in healthy subjects. The IL-4 delta 2 expression was lower in cag-PAI-positive than in cag-PAI-negative H. pylori infected patients. AGS cells also produced IL-4 mRNA upon SSI strain stimulation, whereas IL-4 delta 2 mRNA expression was detected in AGS co-cultured with either SS] or B128 strains. An inverse correlation was documented between IL-4 and IL-4 delta 2 mRNA expression by microdissected gastric epithelial cells and the score of gastritis. IL-4, but not IL-4 delta 2, is expressed by gastric epithelium of healthy subjects, whereas IL-4 delta 2 and lesser IL-4 mRNA are detectable in the gastric epithelium of H. pylori-infected patients. Data suggest that gastric epithelial cells might regulate the balance between tolerance and immune response by the fine tuning of IL-4 and IL-4 delta 2 expression.