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在血行性葡萄球菌和链球菌分离株中,对血小板杀菌蛋白的体外耐药性与心内膜炎来源相关。

In vitro resistance to platelet microbicidal protein correlates with endocarditis source among bacteremic staphylococcal and streptococcal isolates.

作者信息

Wu T, Yeaman M R, Bayer A S

机构信息

Department of Microbiology, California State University, Long Beach 90840.

出版信息

Antimicrob Agents Chemother. 1994 Apr;38(4):729-32. doi: 10.1128/AAC.38.4.729.

Abstract

Traditionally, platelets have been thought to contribute to the induction and propagation of infective endocarditis (IE). However, recent studies suggest that platelets may potentially mitigate IE via secretion of alpha-granule-derived platelet microbicidal protein (PMP). In this study, we compared the PMP susceptibility of bacteremic isolates from patients with and without IE. Isolates of Staphylococcus aureus (n = 17), coagulase-negative staphylococci (CNS; n = 28), viridans streptococci (VS; n = 54), and Enterococcus faecalis (n = 20), each at a final inoculum of 2 x 10(3) CFU/ml, were exposed to PMP [100 U/ml, (5 micrograms/ml)] for 2 h, and the percent survival was determined. For S. aureus, CNS, and VS isolates, there was a significant correlation between an IE source and increased percent survival post-PMP exposure; the mean percent survivals of S. aureus, CNS, and VS were significantly greater for IE versus non-IE isolates (P < 0.005 for each organism). No significant correlation was observed between the source of bacteremic E. faecalis isolates and PMP susceptibility. These data suggest that staphylococcal and VS (but not enterococcal) resistance to PMP may facilitate either the induction or progression of IE.

摘要

传统上,血小板被认为有助于感染性心内膜炎(IE)的诱导和传播。然而,最近的研究表明,血小板可能通过分泌α-颗粒衍生的血小板杀菌蛋白(PMP)来减轻IE。在本研究中,我们比较了有IE和无IE患者血培养分离菌对PMP的敏感性。金黄色葡萄球菌(n = 17)、凝固酶阴性葡萄球菌(CNS;n = 28)、草绿色链球菌(VS;n = 54)和粪肠球菌(n = 20)的分离菌,终浓度均为2×10³CFU/ml,分别暴露于PMP [100 U/ml,(5 μg/ml)] 2小时,然后测定存活率。对于金黄色葡萄球菌、CNS和VS分离菌,IE来源与PMP暴露后存活率增加之间存在显著相关性;与非IE分离菌相比,IE患者的金黄色葡萄球菌、CNS和VS的平均存活率显著更高(每种菌P < 0.005)。在粪肠球菌血培养分离菌的来源与PMP敏感性之间未观察到显著相关性。这些数据表明,葡萄球菌和VS(但不是肠球菌)对PMP的耐药性可能促进IE的诱导或进展。

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