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;
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
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
- Helicobacter pylori
- molecular biology
Funding This work was supported by the Karoji Memorial Fund for Medical Research in Hirosaki University (TI).
Competing interests None.
Patient consent Obtained.
Ethics approval The study was approved by the Committee of Medical Ethics of Hirosaki University Graduate School of Medicine.
Provenance and peer review Not commissioned; externally peer reviewed.