Human beta-defensin-3 induction in H pylori-infected gastric mucosal tissues.
AIM: To examine human beta-defensin-3 (hBD-3) expression in inflamed gastric mucosal tissues or MKN45 gastric cancer cells with or without H pylori infection for better understanding the innate immune response to H pylori. METHODS: We used reverse transcription-polymerase chain reactions and immunohistochemistry to examine hBD-3 expression in inflamed gastric mucosal tissues or MKN45 gastric cancer cells with or without H pylori. Effects of hBD-3 against H pylori were also evaluated. RESULTS: The mean mRNA expression of hBD-3 in H pylori-positive specimens was significantly higher than that in H pylori-negative specimens (P = 0.0002, Mann-Whitney). In addition, unlike uninfected samples, 8 of 15 (53.33%) infected mucosal samples expressed hBD-3 protein. H pylori dose-dependently induced mRNA expression of hBD-3 in MKN45 cells, an effect inhibited by adding anti-toll-like receptor (TLR)-4 antibody. HBD-3 protein completely inhibited H pylori growth. CONCLUSION: Our results suggest that like hBD-2, hBD-3 may be involved in the pathophysiology of H pylori-induced gastritis.[1]References
- Human beta-defensin-3 induction in H pylori-infected gastric mucosal tissues. Kawauchi, K., Yagihashi, A., Tsuji, N., Uehara, N., Furuya, D., Kobayashi, D., Watanabe, N. World J. Gastroenterol. (2006) [Pubmed]
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