期刊
JOURNAL OF INFECTIOUS DISEASES
卷 196, 期 9, 页码 1386-1393出版社
OXFORD UNIV PRESS INC
DOI: 10.1086/522520
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Background. The cytokines induced by Helicobacter pylori, as well as the intricate balance of proinflammatory and anti-inflammatory cytokines, are relevant to the outcomes of H. pylori infection. Transforming growth factor (TGF)-beta and interleukin (IL)-10 are 2 vital anti-inflammatory cytokines that regulate mucosal immunity in various inflammatory and infectious diseases. Methods. To elucidate whether host-bacteria interaction can influence TGF-beta and IL-10 production, we investigated the expression of TGF-beta and IL-10 in various mammalian cell lines preincubated with H. pylori and other enteric bacteria. Results. The amount of TGF-beta protein, but not IL-10, was significantly increased after stimulation with H. pylori, but other enteric bacteria did not induce TGF-beta production. Different H. pylori strains isolated from patients with gastritis, peptic ulcer, gastric cancer and strains with cagA or vacA isogenic mutations showed similar effects on TGF-beta induction, indicating that this effect was a constitutional characteristic of H. pylori and independent of cagA and vacA status. Conclusion. The results imply the presence of a protein factor ( termed TGF-beta-inducing protein) that induces production of TGF-beta. In view of the multiple effects of TGF-beta, we conclude the TGF-beta-inducing protein of H. pylori might mediate the immune response and contribute to the pathogenesis of H. pylori infection.
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