Literature DB >> 18958622

Effect of RANTES promoter genotype on the severity of intestinal metaplasia in Helicobacter pylori-infected Japanese subjects.

Tomomitsu Tahara1, Tomiyasu Arisawa, Tomoyuki Shibata, Masakatsu Nakamura, Hiromi Yamashita, Daisuke Yoshioka, Masaaki Okubo, Naoko Maruyama, Toshiaki Kamano, Yoshio Kamiya, Hiroshi Fujita, Mitsuo Nagasaka, Masami Iwata, Kazuya Takahama, Makoto Watanabe, Hiroshi Nakano, Ichiro Hirata.   

Abstract

BACKGROUND: A complex interaction of host genetic and environmental factors may be relevant in the development of Helicobacter pylori (H. pylori)-related gastro-duodenal diseases. RANTES is a potent chemoattractant peptide for memory T lymphocytes and eosinophils, and has been shown to be enhanced in H. pylori-infected gastric mucosa. We aimed to clarify the effect of RANTES functional promoter polymorphism on the risk of gastro-duodenal diseases in a Japanese population.
METHODS: Four hundred and eighty-three subjects, comprising 106 gastric ulcer, 52 duodenal ulcer, and 325 non-ulcer subjects, were included in this study. Restriction fragment length polymorphism (RFLP) analysis was performed for polymorphisms at -28 C/G in the RANTES gene promoter region. Gastritis scores of antral gastric mucosa were assessed according to the updated Sydney system.
RESULTS: There were no significant differences in the RANTES promoter genotype distributions among non-ulcer subjects, ulcer patients, and gastric and duodenal ulcers. However, the degree of intestinal metaplasia was significantly lower among G carriers in H. pylori-infected subjects aged 60 years or older (C/C vs. G carriers; 1.28 +/- 1.02 vs. 0.83 +/- 0.89, P = 0.0357). In addition, we also found that the same genotype held a lower risk of more severe intestinal metaplasia in H. pylori-infected female subjects (C/C vs. G carriers; 0.91 +/- 1.03 vs. 0.41 +/- 0.73, P = 0.0443).
CONCLUSION: The polymorphism of RANTES promoter is not associated with the susceptibility to peptic ulcer diseases, but the -28 G carrier is associated with a reduced risk of developing more severe intestinal metaplasia in H. pylori-positive subjects aged 60 years and older and in female subjects.

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Year:  2008        PMID: 18958622     DOI: 10.1007/s10620-008-0497-2

Source DB:  PubMed          Journal:  Dig Dis Sci        ISSN: 0163-2116            Impact factor:   3.199


  28 in total

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Journal:  Gut       Date:  2005-06       Impact factor: 23.059

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Authors:  Kunihiro Nakajima; Yasushi Tanaka; Takashi Nomiyama; Takeshi Ogihara; Fuki Ikeda; Rei Kanno; Noseki Iwashita; Ken Sakai; Hirotaka Watada; Tomio Onuma; Ryuzo Kawamori
Journal:  Diabetes Care       Date:  2003-03       Impact factor: 19.112

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Journal:  Scand J Immunol       Date:  1993-01       Impact factor: 3.487

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Journal:  Gut       Date:  1998-05       Impact factor: 23.059

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1.  Telomere length in non-neoplastic gastric mucosa and its relationship to H. pylori infection, degree of gastritis, and NSAID use.

Authors:  Tomomitsu Tahara; Tomoyuki Shibata; Tomohiko Kawamura; Takamitsu Ishizuka; Masaaki Okubo; Mitsuo Nagasaka; Yoshihito Nakagawa; Tomiyasu Arisawa; Naoki Ohmiya; Ichiro Hirata
Journal:  Clin Exp Med       Date:  2015-01-07       Impact factor: 3.984

2.  Inflammatory cytokine gene polymorphisms increase the risk of atrophic gastritis and intestinal metaplasia.

Authors:  Zhong-Wu Li; Ying Wu; Yu Sun; Lu-Ying Liu; Meng-Meng Tian; Guo-Shuang Feng; Wei-Cheng You; Ji-You Li
Journal:  World J Gastroenterol       Date:  2010-04-14       Impact factor: 5.742

3.  Interleukin 33 Triggers Early Eosinophil-Dependent Events Leading to Metaplasia in a Chronic Model of Gastritis-Prone Mice.

Authors:  Carlo De Salvo; Luca Pastorelli; Christine P Petersen; Ludovica F Buttò; Kristine-Ann Buela; Sara Omenetti; Silviu A Locovei; Shuvra Ray; Hannah R Friedman; Jacob Duijser; Wei Xin; Abdullah Osme; Fabio Cominelli; Ganapati H Mahabeleshwar; Jason C Mills; James R Goldenring; Theresa T Pizarro
Journal:  Gastroenterology       Date:  2020-10-01       Impact factor: 22.682

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