Gut and Liver 2010; 4(1): 43-53 https://doi.org/10.5009/gnl.2010.4.1.43 Suppressed Gastric Mucosal TGF-Ղ1 Increases Susceptibility to H. pylori-Induced Gastric Inflammation and Ulceration: A Stupid Host Defense Response
Author Information
Yunjeong Jo*, Sang Uk Han, Yoon Jae Kim*, Ju Hyeon Kim*, Shin Tae Kim*, Seong-Jin Kim*, and Ki-Baik Hahm*
*Laboratory of Cell Regulation and Carcinogenesis, Lee Gil Ya Cancer and Diabetes Institute, Gachon University of Medicine and Science, Incheon, and Department of Surgery, Ajou University School of Medicine, Suwon, Korea

Ki-Baik Hahm
© The Korean Society of Gastroenterology, the Korean Society of Gastrointestinal Endoscopy, the Korean Society of Neurogastroenterology and Motility, Korean College of Helicobacter and Upper Gastrointestinal Research, Korean Association the Study of Intestinal Diseases, the Korean Association for the Study of the Liver, Korean Pancreatobiliary Association, and Korean Society of Gastrointestinal Cancer. All rights reserved.

Abstract
Background/Aims: Loss of transforming growth factor Ղ1 (TGF-Ղ1) 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-Ղ1 levels could be used to determine the outcome after H. pylori infection. Methods: Northern blot for the TGF-Ղ1 transcript, staining of TGF-Ղ1 expression, luciferase reporter assay, and enzyme-linked immunosorbent assay for TGF-Ղ1 levels were performed at different times after H. pylori infection. Results: The TGF-Ղ1 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-Ղ1 levels. SNU-16 cells showing intact TGF-Ղ signaling exhibited a marked decrease in TGF-Ղ1 expression, whereas SNU-638 cells defective in TGF-Ղ signaling exhibited no such decrease after H. pylori infection. The decreased expressions of TGF-Ղ1 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-Ղ1 is a host defense mechanism to avoid attachment of H. pylori. Conclusions: H. pylori infection was associated with depressed gastric mucosal TGF-Ղ1 for up to 24 hr, but this apparent strategy for rescuing cells from H. pylori attachment exacerbated the gastric inflammation. (Gut Liver 2010;4:43-53)
Keywords: Helicobacter pylori; TGF-Ղ; Inflammation; Ulcer; Host defense
Abstract
Background/Aims: Loss of transforming growth factor Ղ1 (TGF-Ղ1) 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-Ղ1 levels could be used to determine the outcome after H. pylori infection. Methods: Northern blot for the TGF-Ղ1 transcript, staining of TGF-Ղ1 expression, luciferase reporter assay, and enzyme-linked immunosorbent assay for TGF-Ղ1 levels were performed at different times after H. pylori infection. Results: The TGF-Ղ1 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-Ղ1 levels. SNU-16 cells showing intact TGF-Ղ signaling exhibited a marked decrease in TGF-Ղ1 expression, whereas SNU-638 cells defective in TGF-Ղ signaling exhibited no such decrease after H. pylori infection. The decreased expressions of TGF-Ղ1 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-Ղ1 is a host defense mechanism to avoid attachment of H. pylori. Conclusions: H. pylori infection was associated with depressed gastric mucosal TGF-Ղ1 for up to 24 hr, but this apparent strategy for rescuing cells from H. pylori attachment exacerbated the gastric inflammation. (Gut Liver 2010;4:43-53)
Keywords: Helicobacter pylori; TGF-Ղ; Inflammation; Ulcer; Host defense
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