Slomiany B L, Piotrowski J, Slomiany A
Research Center, University of Medicine and Dentistry of New Jersey, Newark, New Jersey, 07103-2400, USA.
Biochem Biophys Res Commun. 1999 Apr 29;258(1):17-20. doi: 10.1006/bbrc.1999.0578.
In this study, we investigated gastric mucosal inflammatory responses during Helicobacter pylori lipopolysaccharide-induced gastritis by analyzing the interplay between mucosal expression of endothelin-1 (ET-1), interleukin-4 (IL-4) and tumor necrosis factor-alpha (TNF-alpha). The assays conducted 4 days after intragastric dose of H. pylori lipopolysaccharide demonstrated a pattern of acute mucosal reaction characterized by the inflammatory infiltration of the lamina propria, hyperemia, and epithelial hemorrhage. This was accompanied by a 3.1-fold increase in the mucosal expression of ET-1 and a 9-fold enhancement in TNF-alpha, while the level of IL-4 showed a 20.8% decline. The results implicate ET-1 in gastric mucosal responses to H. pylori, and suggest that an increase in its level, combined with a loss of compensatory action by IL-4, may be responsible for the induction of TNF-alpha and triggering apoptotic events that exacerbate the inflammatory process.
在本研究中，我们通过分析内皮素-1（ET-1）、白细胞介素-4（IL-4）和肿瘤坏死因子-α（TNF-α）在胃黏膜中的表达相互作用，研究了幽门螺杆菌脂多糖诱导胃炎期间的胃黏膜炎症反应。在胃内给予幽门螺杆菌脂多糖4天后进行的检测显示出一种急性黏膜反应模式，其特征为固有层炎症浸润、充血和上皮出血。这伴随着ET-1的黏膜表达增加3.1倍以及TNF-α增强9倍，而IL-4水平下降了20.8%。结果表明ET-1参与胃黏膜对幽门螺杆菌的反应，并提示其水平升高，加上IL-4代偿作用的丧失，可能是诱导TNF-α和引发加剧炎症过程的凋亡事件的原因。
