Abstract | BACKGROUND: 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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Authors | Ming-Shiang Wu, Jaw-Town Lin, Ping-Ning Hsu, Ching-Yi Lin, Yuan-Ting Hsieh, Yi-Han Chiu, Po-Ren Hsueh, Kuang-Wen Liao |
Journal | The Journal of infectious diseases
(J Infect Dis)
Vol. 196
Issue 9
Pg. 1386-93
(Nov 01 2007)
ISSN: 0022-1899 [Print] United States |
PMID | 17922404
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antigens, Bacterial
- Bacterial Proteins
- Transforming Growth Factor beta
- VacA protein, Helicobacter pylori
- cagA protein, Helicobacter pylori
- Interleukin-10
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Topics |
- Antigens, Bacterial
(genetics, metabolism)
- Bacterial Proteins
(chemistry, genetics, metabolism)
- Cell Line, Tumor
- Epithelial Cells
(metabolism)
- Helicobacter pylori
(metabolism)
- Humans
- Interleukin-10
(metabolism)
- Monocytes
(metabolism)
- Stomach
(cytology)
- Transforming Growth Factor beta
(biosynthesis)
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