Expression of melanoma differentiation associated gene 5 is increased in human gastric mucosa infected with Helicobacter pylori
- Tetsuya Tatsuta1,
- Tadaatsu Imaizumi2,
- Tadashi Shimoyama1,
- Manabu Sawaya1,
- Tanji Kunikazu3,
- Tomoh Matsumiya2,
- Hidemi Yoshida2,
- Kei Satoh2,
- Shinsaku Fukuda1
- 1Department of Gastroenterology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan
- 2Department of Vascular Biology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan
- 3Department of Neuropathology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan
- Correspondence to Tadashi Shimoyama, Department of Gastroenterology, Hirosaki University Graduate School of Medicine, 5 Zaifu-cho, Hirosaki 036-8562, Japan; tsimo-hki{at}umin.ac.jp
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Contributors Drs Koichi Wakabayashi, Michiko Nakata and Kumiko Munakata helped in RNA extraction and immunohistochemical examination. They also attended the discussion for this paper.
- Accepted 2 March 2012
- Published Online First 29 March 2012
Abstract
Helicobacter pylori infection is associated with gastroduodenal diseases. Melanoma differentiation associated gene 5 (MDA5) plays a role in antiviral host defense. We investigated the effect of H pylori infection on MDA5 expression in human gastric mucosa. Biopsy samples from the antrum and corpus were obtained from 33 patients. MDA5 mRNA and protein were examined by real-time PCR and immunohistochemical staining. Histological gastritis was graded according to updated Sydney System. MDA5 mRNA was significantly increased in the antrum infected with H pylori. MDA5 protein positively stained in infiltrating mononuclear cells. MDA5 mRNA expression was significantly correlated with the grade of glandular atrophy (rs = 0.767) and intestinal metaplasia (rs = 0.748) in the corpus with H pylori infection. These results indicate that MDA5 may be involved in innate immune reactions against H pylori and associate with glandular atrophy and intestinal metaplasia in patients with H pylori infection.
- Cell biology
- gastric cancer
- gastritis
- Helicobacter pylori
- immunology
- immunopathology
- inflammation
- molecular biology
- neurodegeneration
- nutrition
- stroke
Footnotes
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Funding This work was supported by the Karoji Memorial Fund for Medical Research in Hirosaki University (TI).
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Competing interests None.
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Patient consent Obtained.
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Ethics approval The study was approved by the Committee of Medical Ethics of Hirosaki University Graduate School of Medicine.
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Provenance and peer review Not commissioned; externally peer reviewed.








