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  • 1. Aims and Scope

    Gut and Liver is an international journal of gastroenterology, focusing on the gastrointestinal tract, liver, biliary tree, pancreas, motility, and neurogastroenterology. Gut atnd Liver delivers up-to-date, authoritative papers on both clinical and research-based topics in gastroenterology. The Journal publishes original articles, case reports, brief communications, letters to the editor and invited review articles in the field of gastroenterology. The Journal is operated by internationally renowned editorial boards and designed to provide a global opportunity to promote academic developments in the field of gastroenterology and hepatology. +MORE

  • 2. Editorial Board

    Editor-in-Chief + MORE

    Editor-in-Chief
    Yong Chan Lee Professor of Medicine
    Director, Gastrointestinal Research Laboratory
    Veterans Affairs Medical Center, Univ. California San Francisco
    San Francisco, USA

    Deputy Editor

    Deputy Editor
    Jong Pil Im Seoul National University College of Medicine, Seoul, Korea
    Robert S. Bresalier University of Texas M. D. Anderson Cancer Center, Houston, USA
    Steven H. Itzkowitz Mount Sinai Medical Center, NY, USA
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    All papers submitted to Gut and Liver are reviewed by the editorial team before being sent out for an external peer review to rule out papers that have low priority, insufficient originality, scientific flaws, or the absence of a message of importance to the readers of the Journal. A decision about these papers will usually be made within two or three weeks.
    The remaining articles are usually sent to two reviewers. It would be very helpful if you could suggest a selection of reviewers and include their contact details. We may not always use the reviewers you recommend, but suggesting reviewers will make our reviewer database much richer; in the end, everyone will benefit. We reserve the right to return manuscripts in which no reviewers are suggested.

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Suppressed Gastric Mucosal TGF-Ղ1 Increases Susceptibility to H. pylori-Induced Gastric Inflammation and Ulceration: A Stupid Host Defense Response

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

Correspondence to: Ki-Baik Hahm

Gut Liver 2010;4(1):43-53. https://doi.org/10.5009/gnl.2010.4.1.43

Published online November 30, -0001, Published date March 30, 2010

Copyright © Gut and Liver.

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


Article

Review

Gut and Liver 2010; 4(1): 43-53

Published online March 30, 2010 https://doi.org/10.5009/gnl.2010.4.1.43

Copyright © Gut and Liver.

Suppressed Gastric Mucosal TGF-Ղ1 Increases Susceptibility to H. pylori-Induced Gastric Inflammation and Ulceration: A Stupid Host Defense Response

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

Correspondence to:Ki-Baik Hahm

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

Gut and Liver

Vol.18 No.3
May, 2024

pISSN 1976-2283
eISSN 2005-1212

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