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KMID : 1188320100040010043
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Gut and Liver
2010 Volume.4 No. 1 p.43 ~ p.53
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Suppressed Gastric Mucosal TGF-?1 Increases Susceptibility to H. pylori-Induced Gastric Inflammation and Ulceration: A Stupid Host Defense Response
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Jo Yun-Jeong
Han Sang-Uk
Kim Yoon-Jae
Kim Ju-Hyeon
Kim Shin-Tae
Kim Seong-Jin
Hahm Ki-Baik
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Abstract
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Background/Aims: Loss of transforming growth factor ?1 (TGF-?1) exhibits a similar pathology to that seen in a subset of individuals infected with Helicobacter pylori, including propagated gastric inflammation, oxidative stress, and autoimmune features. We thus hypothesized that gastric mucosal TGF-?1 levels could be used to determine the outcome after H. pylori infection.
Methods: Northern blot for the TGF-?1 transcript, staining of TGF-?1 expression, luciferase reporter assay, and enzyme-linked immunosorbent assay for TGF-?1 levels were performed at different times after H. pylori infection.
Results: The TGF-?1 level was markedly lower in patients with H. pylori-induced gastritis than in patients with a similar degree of gastritis induced by nonsteroidal anti-inflammatory drugs. There was a significant negative correlation between the severity of inflammation and gastric mucosal TGF-?1 levels. SNU-16 cells showing intact TGF-? signaling exhibited a marked decrease in TGF-?1 expression, whereas SNU-638 cells defective in TGF-? signaling exhibited no such decrease after H. pylori infection. The decreased expressions of TGF-?1 in SNU-16 cells recovered to normal after 24 hr of H. pylori infection, but lasted very spatial times, suggesting that attenuated expression of TGF-?1 is a host defense mechanism to avoid attachment of H. pylori.
Conclusions: H. pylori infection was associated with depressed gastric mucosal TGF-?1 for up to 24 hr, but this apparent strategy for rescuing cells from H. pylori attachment exacerbated the gastric inflammation.
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KEYWORD
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Helicobacter pylori, TGF-?, Inflammation, Ulcer, Host defense
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