Wallace J L, Granger D N
Intestinal Disease Research Unit, University of Calgary, Alberta, Canada.
FASEB J. 1996 May;10(7):731-40. doi: 10.1096/fasebj.10.7.8635690.
The association between colonization of the stomach by Helicobacter pylori and peptic ulcer disease has stimulated a renewal of interest in the factors that render the gastric mucosa resistant to injury induced by endogenous secretions and ingested toxins. Mucosal defense consists of a complex network of components that function in concert with one another. This network includes: 1) the extramucosal components such as acid, mucus, surface-active phospholipids, and bicarbonate; 2) the epithelium itself; 3) the microcirculation and sensory afferent neurons beneath the epithelium; 4) the mucosal immune system; and 5) the ability of the mucosa to undergo repair. In the past two decades, an enormous amount has been learned about the cellular and molecular basis of the various components of mucosal defense, including a better understanding of the chemical substances that coordinate mucosal responses to injury. In this paper, we review the factors that contribute to mucosal defense, the cellular and molecular mechanisms through which mucosal defense is modulated, and the chemical mediators that play key roles in this process.
幽门螺杆菌在胃内定植与消化性溃疡病之间的关联,激发了人们对使胃黏膜抵抗内源性分泌物和摄入毒素所致损伤的因素的新一轮研究兴趣。黏膜防御由相互协同发挥作用的复杂成分网络组成。该网络包括:1)黏膜外成分,如胃酸、黏液、表面活性磷脂和碳酸氢盐;2)上皮本身;3)上皮下方的微循环和感觉传入神经元;4)黏膜免疫系统;5)黏膜的修复能力。在过去二十年中,人们对黏膜防御各成分的细胞和分子基础有了大量了解,包括对协调黏膜损伤反应的化学物质有了更深入的认识。在本文中,我们综述了有助于黏膜防御的因素、调节黏膜防御的细胞和分子机制,以及在此过程中起关键作用的化学介质。