O'Brien Mauria
University of Illinois Urbana-Champaign, College of Veterinary Medicine, Urbana, IL 61802, USA.
Top Companion Anim Med. 2012 May;27(2):46-52. doi: 10.1053/j.tcam.2012.06.003. Epub 2012 Aug 2.
Inflammation and coagulation constitute two host defense systems with complementary roles in eliminating invading pathogens, limiting tissue damage, and restoring homeostasis. Extensive cross talk exists between these 2 systems, whereby inflammation leads to activation of coagulation, and coagulation considerably affects inflammatory activity. Infection leads to the production of proinflammatory cytokines that, in turn, stimulate the production of tissue factor. Activation of the coagulation system and ensuing thrombin generation are dependent on the expression of tissue factor. Conversely, activated coagulation proteases may affect specific receptors on inflammatory cells and endothelial cells and thereby modulate the inflammatory response. Activation of coagulation with the simultaneous down-regulation of endothelial-bound anticoagulant mechanisms and endogenous fibrinolysis characterizes the pathophysiology of sepsis. The mechanisms by which these highly complex and codependent defense strategies are linked together both in health and disease is the focus of this review.
炎症和凝血构成了两个宿主防御系统，它们在消除入侵病原体、限制组织损伤和恢复体内平衡方面发挥着互补作用。这两个系统之间存在广泛的相互作用，炎症会导致凝血激活，而凝血会显著影响炎症活动。感染会导致促炎细胞因子的产生，进而刺激组织因子的产生。凝血系统的激活以及随后的凝血酶生成依赖于组织因子的表达。相反，活化的凝血蛋白酶可能会影响炎症细胞和内皮细胞上的特定受体，从而调节炎症反应。凝血激活同时伴有内皮结合抗凝机制和内源性纤维蛋白溶解的下调，这是脓毒症病理生理学的特征。在健康和疾病状态下，这些高度复杂且相互依赖的防御策略相互关联的机制是本综述的重点。
