Mandic-Mulec I, Weiss J, Zychlinsky A
The Skirball Institute, New York University School of Medicine, New York, New York 10016, USA.
Infect Immun. 1997 Jan;65(1):110-5. doi: 10.1128/iai.65.1.110-115.1997.
We examined the bactericidal activity of polymorphonuclear leukocytes (PMN) against an invasive wild-type strain of Shigella flexneri (M90T) and a plasmid-cured noninvasive derivative (BS176). Both Shigella strains, as well as a rough strain of Escherichia coli, were killed with similar efficiencies by intact inflammatory PMN in room air and under N2 (i.e., killing was O2 independent). Bacterial killing by PMN extracts was substantially inhibited by antibodies to the bactericidal/permeability-increasing protein (BPI). Whereas wild-type Shigella escapes from the phagosome to the cytoplasm in epithelial cells and macrophages, wild-type Shigella was trapped in the phagolysosome of PMN as visualized by electron microscopy. The efficient killing of Shigella by PMN suggests that these inflammatory cells may not only contribute initially to the severe tissue damage characteristic of shigellosis but also ultimately participate in clearance and resolution of infection.
我们检测了多形核白细胞(PMN)对侵袭性野生型福氏志贺菌(M90T)和质粒消除的非侵袭性衍生物(BS176)的杀菌活性。在室内空气和氮气环境下,完整的炎性PMN对这两种志贺菌菌株以及一株粗糙型大肠杆菌的杀灭效率相似(即杀灭作用不依赖氧气)。PMN提取物的杀菌作用被抗杀菌/通透性增加蛋白(BPI)抗体显著抑制。野生型志贺菌在上皮细胞和巨噬细胞中可从吞噬体逃逸至细胞质,但通过电子显微镜观察发现,野生型志贺菌被困在PMN的吞噬溶酶体中。PMN对志贺菌的有效杀灭表明,这些炎性细胞不仅可能最初导致志贺菌病特有的严重组织损伤,而且最终可能参与感染的清除和消退。