Etiopathogenesis of inflammatory bowel diseases

理论解释煽动性的肠疾病(IBD ) 的发病机理自从 Crohn 的疾病(CD ) 和 ulcerative (UC ) 被建议了作为疾病的二种主要形式被认出。尽管在 CD 和 UC 的织物损坏的准确原因和机制还得完全被理解，足够的进步发生了作为有效接受下列假设：IBD 是在环境因素，微生物引起的因素，和肠的免疫系统之中作为一个复杂相互作用的结果发生在遗传上易受影响的个人的不恰当的有免疫力的回答。在环境因素的一张几乎无穷的表之中，吸烟为 UC 为 CD 和一个保护的因素作为一个风险因素被识别了。在微生物引起的因素之中，没有有说服力的证据显示古典传染代理人引起 IBD，当作为具有中央重要性对正常伤寒植物群装证据点到反常有免疫力的回答时。内脏发炎被天生以及适应的免疫系统的房间调停，与非有免疫力的房间的另外的贡献，例如上皮，间充质并且 endothelial，和血小板。

Theories explaining the etiopathogenesis of inflammatory bowel disease （IBD） have been proposed ever since Crohn＇s disease （CD） and ulcerative colitis （UC） were recognized as the two major forms of the disease. Although the exact cause（s） and mechanisms of tissue damage in CD and UC have yet to be completely understood, enough progress has occurred to accept the following hypothesis as valid： IBD is an inappropriate immune response that occurs in genetically susceptible individuals as the result of a complex interaction among environmental factors, microbial factors, and the intestinal immune system. Among an almost endless list of environmental factors, smoking has been identified as a risk factor for CD and a protective factor for UC. Among microbial factors, no convincing evidence indicates that classical infectious agents cause IBD, while mounting evidence points to an abnormal immune response against the normal enteric flora as being of central importance. Gut inflammation is mediated by cells of the innate as well as adaptive immune systems, with the additional contribution of non-immune cells, such as epithelial, mesenchymal and endothelial cells, and platelets.