Kapral F A
J Bacteriol. 1966 Oct;92(4):1188-95. doi: 10.1128/jb.92.4.1188-1195.1966.
Kapral, Frank A. (Philadelphia General Hospital, Philadelphia, Pa.). Clumping of Staphylococcus aureus in the peritoneal cavity of mice. J. Bacteriol. 92:1188-1195. 1966.-Nonencapsulated strains of Staphylococcus aureus inoculated into the peritoneal cavity of mice are promptly clumped by the interaction of fibrinogen with the bound coagulase present on the bacterial surface. Some of the pre-existing leukocytes adhere to the staphylococcal clumps during the 1st hr, but phagocytosis is minimal. During the 2nd hr, there is an influx of neutrophils into the region, and these form a thick layer around the staphylococcal clumps and, apparently, prevent further egress of toxin. Leukocytes in proximity to the organisms undergo degeneration, but cells located externally maintain an effective barrier and, thus, confine the organisms. The encapsulated Smith strain of S. aureus is not clumped under these circumstances, presumably because the capsule prevents the bound coagulase-fibrinogen interaction.
卡普拉尔,弗兰克·A.(宾夕法尼亚州费城综合医院)。小鼠腹腔内金黄色葡萄球菌的聚集。《细菌学杂志》92:1188 - 1195。1966年。-接种到小鼠腹腔内的非包膜金黄色葡萄球菌菌株会因纤维蛋白原与细菌表面结合的凝固酶相互作用而迅速聚集。在最初1小时内,一些预先存在的白细胞会黏附在葡萄球菌聚集体上,但吞噬作用很微弱。在第2小时,中性粒细胞流入该区域,它们在葡萄球菌聚集体周围形成一层厚厚的层,显然阻止了毒素的进一步释放。靠近细菌的白细胞会发生变性,但位于外部的细胞维持着有效的屏障,从而限制了细菌。在这些情况下,包膜的金黄色葡萄球菌史密斯菌株不会聚集,推测是因为包膜阻止了结合的凝固酶 - 纤维蛋白原相互作用。