Katz J A, Itoh J, Fiocchi C
Division of Gastroenterology, University Hospitals of Cleveland, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA.
Curr Opin Gastroenterol. 1999 Jul;15(4):291-7. doi: 10.1097/00001574-199907000-00003.
In spite of expanding knowledge of cellular and molecular mechanisms of intestinal inflammation, the etiology and pathogenesis of inflammatory bowel disease (IBD) remain obscure. The link between the environment and IBD is still circumstantial, but definite progress is occurring in defining genetic susceptibility loci for Crohn's disease (CD) and ulcerative colitis (UC). The notion that normal enteric flora play a role in initiating or maintaining IBD is gaining momentum. Some components of the flora may act as noxious agents, whereas others (probiotics) seem to have a protective effect. The importance of the mucosal immune system to IBD is established, and evidence is accumulating that nonimmune components, such as epithelial, mesenchymal, and endothelial cells, also contribute to gut inflammation. The effect of cytokines in intestinal immunity is being elucidated by studies on their molecular mechanism, particularly the activation of nuclear factor (NF)-kappaB. Finally, the beneficial effects of cytoprotective prostaglandins and cell adhesion molecule (CAM) blockade promise novel therapeutic opportunities derived from an improved understanding of IBD pathogenesis.
尽管对肠道炎症的细胞和分子机制的认识不断扩展，但炎症性肠病（IBD）的病因和发病机制仍不清楚。环境与IBD之间的联系仍然是间接的，但在确定克罗恩病（CD）和溃疡性结肠炎（UC）的遗传易感性位点方面正取得明确进展。正常肠道菌群在引发或维持IBD中起作用这一观点正越来越受到关注。菌群的某些成分可能作为有害物质起作用，而其他成分（益生菌）似乎具有保护作用。黏膜免疫系统对IBD的重要性已得到确立，并且越来越多的证据表明，上皮细胞、间充质细胞和内皮细胞等非免疫成分也会导致肠道炎症。关于细胞因子在肠道免疫中的作用，正通过对其分子机制的研究加以阐明，尤其是核因子（NF）-κB的激活。最后，细胞保护性前列腺素和细胞黏附分子（CAM）阻断的有益作用有望带来基于对IBD发病机制更好理解的新治疗机会。
