Danese Silvio
Division of Gastroenterology, Laboratory of Inflammation and Immunology, IRCCS Istituto Clinico Humanitas, Rozzano, Milan, Italy.
Curr Opin Gastroenterol. 2007 Jul;23(4):384-9. doi: 10.1097/MOG.0b013e32810c8de3.
Inflammatory bowel disease pathogenesis involves the interplay of multiple biological factors, among which nonimmune cells, including the endothelium, represent a crucial component of disease pathogenesis.
Endothelial cells play a key role in chronic inflammation through multiple and disparate activities. The mucosal microvasculature in inflammatory bowel disease is dysfunctional, overexpresses inflammatory molecules and undergoes intense angiogenesis, failing to exert its physiological antiinflammatory and anticoagulant activities.
The mucosal microcirculation is abnormal in inflammatory bowel disease and represents a novel component of disease pathogenesis; targeting the various abnormalities of the inflammatory bowel disease microcirculation may lead to new forms of therapeutic intervention.
炎症性肠病的发病机制涉及多种生物学因素的相互作用,其中包括内皮细胞在内的非免疫细胞是疾病发病机制的关键组成部分。
内皮细胞通过多种不同的活动在慢性炎症中起关键作用。炎症性肠病中的黏膜微血管功能失调,炎症分子过度表达,并经历强烈的血管生成,无法发挥其生理抗炎和抗凝活性。
炎症性肠病中黏膜微循环异常,是疾病发病机制的一个新组成部分;针对炎症性肠病微循环的各种异常情况可能会带来新的治疗干预形式。