幽门螺杆菌感染的胃黏膜组织中人类β-防御素-3的诱导作用。
Human beta-defensin-3 induction in H. pylori-infected gastric mucosal tissues.
作者信息
Kawauchi K, Yagihashi A, Tsuji N, Uehara N, Furuya D, Kobayashi D, Watanabe N
机构信息
Department of Clinical Laboratory Medicine, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo 060-8543, Japan.
出版信息
World J Gastroenterol. 2006 Sep 28;12(36):5793-7. doi: 10.3748/wjg.v12.i36.5793.
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.
目的
检测人类β-防御素-3（hBD-3）在幽门螺杆菌感染或未感染的炎症性胃黏膜组织及MKN45胃癌细胞中的表达，以更好地了解对幽门螺杆菌的天然免疫反应。
方法
我们使用逆转录-聚合酶链反应和免疫组织化学方法检测幽门螺杆菌感染或未感染的炎症性胃黏膜组织及MKN45胃癌细胞中hBD-3的表达。还评估了hBD-3对幽门螺杆菌的作用。
结果
幽门螺杆菌阳性标本中hBD-3的平均mRNA表达显著高于幽门螺杆菌阴性标本（P = 0.0002，曼-惠特尼检验）。此外，与未感染样本不同，15个感染的黏膜样本中有8个（53.33%）表达hBD-3蛋白。幽门螺杆菌在MKN45细胞中剂量依赖性地诱导hBD-3的mRNA表达，添加抗Toll样受体（TLR）-4抗体可抑制该效应。hBD-3蛋白完全抑制幽门螺杆菌生长。
结论
我们的结果表明，与hBD-2一样，hBD-3可能参与幽门螺杆菌诱导的胃炎的病理生理过程。
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