Ma T Y
Department of Medicine, DVA Medical Center, Long Beach, California 90822, USA.
Proc Soc Exp Biol Med. 1997 Apr;214(4):318-27. doi: 10.3181/00379727-214-44099.
Despite extensive research, the etiology of Crohn's disease remains unknown. Accumulating evidence suggests the possibility that a primary defect of intestinal barrier function may be present in Crohn's disease. In this review, the possible role of intestinal barrier defect in Crohn's disease is discussed. It has been recognized for some time that Crohn's patients have a defective intestinal epithelial barrier function manifested by an increase in intestinal permeability. Recent studies indicate that a subgroup of healthy first-degree relatives of Crohn's patients (a population at high risk for developing Crohn's disease) also have increased intestinal permeability. Additionally, this subgroup of patients have evidence of increased exposure to foreign antigens, suggesting a possible link between increase in intestinal permeability and increase in antigenic penetration. Furthermore, exacerbation of Crohn's disease is produced by agents that disrupt intestinal epithelial barrier function, while remission of active disease is induced by decreasing intestinal antigenic load. A "leaky gut" hypothesis is advanced which proposes that a preexisting disorder of intestinal permeability is responsible for the intestinal inflammation of Crohn's disease.
尽管进行了广泛的研究，但克罗恩病的病因仍然不明。越来越多的证据表明，克罗恩病可能存在肠道屏障功能的原发性缺陷。在这篇综述中，讨论了肠道屏障缺陷在克罗恩病中可能发挥的作用。一段时间以来，人们已经认识到克罗恩病患者存在肠道上皮屏障功能缺陷，表现为肠道通透性增加。最近的研究表明，克罗恩病患者的健康一级亲属亚组（患克罗恩病的高危人群）也有肠道通透性增加的情况。此外，该亚组患者有接触外来抗原增加的证据，提示肠道通透性增加与抗原渗透增加之间可能存在联系。此外，破坏肠道上皮屏障功能的药物会使克罗恩病病情加重，而降低肠道抗原负荷则可诱导活动期疾病缓解。提出了一个“肠漏”假说，该假说认为，肠道通透性的预先存在的紊乱是克罗恩病肠道炎症的原因。
