Geelen S, Bhattacharyya C, Tuomanen E
Laboratory of Molecular Infectious Diseases, Rockefeller University, New York, New York 10021.
Infect Immun. 1992 Oct;60(10):4179-83. doi: 10.1128/iai.60.10.4179-4183.1992.
The inflammatory response in infection caused by gram-negative organisms involves induction of procoagulant activity (PCA) on human endothelial cells. Although infections caused by gram-positive organisms are also associated with fibrin formation and thrombosis, the bacterial determinants inducing PCA are unknown. This study shows that intact pneumococci and the pneumococcal cell wall efficiently induce PCA on human endothelial cells. Upon exposure of endothelial cells to pneumococci, PCA was first detectable at 30 min, peaked at 2 h, and disappeared by 6 h. The specific activities of encapsulated and unencapsulated strains for induction of PCA were equivalent. Purified pneumococcal cell walls were as potent as endotoxin in induction of PCA. The ability to induce a procoagulant state on endothelial cells is a new biological activity of gram-positive cell walls which promotes the participation of the coagulation cascade in the inflammatory response to disease caused by gram-positive organisms.
革兰氏阴性菌引起的感染中的炎症反应涉及诱导人内皮细胞上的促凝活性(PCA)。尽管革兰氏阳性菌引起的感染也与纤维蛋白形成和血栓形成有关,但诱导PCA的细菌决定因素尚不清楚。本研究表明,完整的肺炎球菌和肺炎球菌细胞壁可有效诱导人内皮细胞上的PCA。内皮细胞暴露于肺炎球菌后,PCA在30分钟时首次可检测到,在2小时时达到峰值,并在6小时时消失。有荚膜和无荚膜菌株诱导PCA的比活性相当。纯化的肺炎球菌细胞壁在诱导PCA方面与内毒素一样有效。在内皮细胞上诱导促凝状态的能力是革兰氏阳性细胞壁的一种新的生物学活性,它促进凝血级联反应参与对革兰氏阳性菌引起的疾病的炎症反应。