MacDonald T T, Murch S H
Medical College of St Bartholomew's Hospital, University of London, West Smithfield, UK.
Baillieres Clin Gastroenterol. 1994 Mar;8(1):1-34. doi: 10.1016/s0950-3528(06)80017-5.
While Crohn's disease and ulcerative colitis are both conditions characterized by intestinal inflammation, with some overlap in their clinical and histological features, they are essentially different in pathogenesis. Crohn's disease appears to be primarily a condition of chronic T-lymphocyte activation, with tissue damage induced by secondary macrophage activation. What activates the T-cells is unknown. In this chapter we look at the evidence for and against cell-wall deficient mycobacteria species, viral infection of vascular endothelium and luminal contents as potential mechanisms of chronic activation. In ulcerative colitis, by contrast, there is no strong evidence for T-cell activation, and humoral mechanisms predominate. While the finding of atypical anti-neutrophil cytoplasmic antibodies (P-ANCAs) may be useful in screening, the only novel pathogenetic discovery is the co-localization of a 40 kD colonic autoantibody with immunoglobulins and complement on the apical enterocyte surface. Despite the fundamental differences in initiating mechanisms, the two conditions have many 'downstream' inflammatory processes in common. We discuss the evidence for local production of cytokines, arachidonic acid metabolites and reactive oxygen and nitrogen radicals, highlighting the potential adverse consequences for intestinal vascular integrity.
虽然克罗恩病和溃疡性结肠炎均以肠道炎症为特征，在临床和组织学特征上有一些重叠，但它们在发病机制上本质不同。克罗恩病似乎主要是一种慢性T淋巴细胞激活的病症，由继发性巨噬细胞激活诱导组织损伤。激活T细胞的因素尚不清楚。在本章中，我们将探讨支持和反对细胞壁缺陷分枝杆菌属、血管内皮细胞病毒感染以及管腔内容物作为慢性激活潜在机制的证据。相比之下，在溃疡性结肠炎中，没有强有力的证据支持T细胞激活，体液机制占主导地位。虽然非典型抗中性粒细胞胞浆抗体（P-ANCA）的发现可能有助于筛查，但唯一新的发病机制发现是一种40kD结肠自身抗体与免疫球蛋白和补体在顶端肠上皮细胞表面的共定位。尽管起始机制存在根本差异，但这两种病症有许多共同的“下游”炎症过程。我们讨论了细胞因子、花生四烯酸代谢产物以及活性氧和氮自由基局部产生的证据，强调了对肠道血管完整性潜在的不良后果。
