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在实验性金黄色葡萄球菌感染性心内膜炎中，对凝血酶诱导的血小板杀菌蛋白的体外抗性与疾病进展加速和血行播散相关。

In vitro resistance to thrombin-induced platelet microbicidal protein is associated with enhanced progression and hematogenous dissemination in experimental Staphylococcus aureus infective endocarditis.

作者信息

Dhawan V K, Bayer A S, Yeaman M R

机构信息

Charles Drew University-Martin Luther King Medical Center, Los Angeles, California 90059, USA.

出版信息

Infect Immun. 1998 Jul;66(7):3476-9. doi: 10.1128/IAI.66.7.3476-3479.1998.

DOI:10.1128/IAI.66.7.3476-3479.1998
PMID:9632628
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC108375/
Abstract

We examined the influence of thrombin-induced platelet microbicidal protein 1 (tPMP-1) on the progression and hematogenous dissemination of experimental endocarditis caused by isogenic Staphylococcus aureus strains differing in tPMP susceptibility (tPMPs) or resistance (tPMPr) in vitro. Following simultaneous challenge of animals with both strains, significantly higher tPMPr bacterial densities were present in vegetations (P < 0.0001), kidneys (P < 0. 0001), and spleens (P < 0.0001) compared with those for the tPMPs strain. These data indicate that tPMP-1 limits the intravegetation proliferation and hematogenous dissemination of a tPMPs strain in experimental endocarditis, while the tPMPr phenotype confers a selective advantage associated with the enhanced progression of this infection.

摘要

我们在体外研究了凝血酶诱导的血小板杀菌蛋白1（tPMP-1）对由tPMP敏感（tPMPs）或耐药（tPMPr）的同基因金黄色葡萄球菌菌株引起的实验性心内膜炎进展和血行播散的影响。在用这两种菌株同时攻击动物后，与tPMPs菌株相比，赘生物（P < 0.0001）、肾脏（P < 0.0001）和脾脏（P < 0.0001）中tPMPr细菌密度显著更高。这些数据表明，tPMP-1限制了实验性心内膜炎中tPMPs菌株在赘生物内的增殖和血行播散，而tPMPr表型赋予了与这种感染进展增强相关的选择性优势。

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In vitro resistance to thrombin-induced platelet microbicidal protein is associated with enhanced progression and hematogenous dissemination in experimental Staphylococcus aureus infective endocarditis.在实验性金黄色葡萄球菌感染性心内膜炎中，对凝血酶诱导的血小板杀菌蛋白的体外抗性与疾病进展加速和血行播散相关。
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本文引用的文献

1
The role of platelets in antimicrobial host defense.血小板在抗菌宿主防御中的作用。
Clin Infect Dis. 1997 Nov;25(5):951-68; quiz 969-70. doi: 10.1086/516120.
2
Phenotypic resistance to thrombin-induced platelet microbicidal protein in vitro is correlated with enhanced virulence in experimental endocarditis due to Staphylococcus aureus.在体外对凝血酶诱导的血小板杀菌蛋白的表型抗性与金黄色葡萄球菌所致实验性心内膜炎中增强的毒力相关。
Infect Immun. 1997 Aug;65(8):3293-9. doi: 10.1128/iai.65.8.3293-3299.1997.
3
Staphylocidal action of thrombin-induced platelet microbicidal protein is influenced by microenvironment and target cell growth phase.凝血酶诱导的血小板杀菌蛋白的杀葡萄球菌作用受微环境和靶细胞生长阶段的影响。
Infect Immun. 1996 Sep;64(9):3758-64. doi: 10.1128/iai.64.9.3758-3764.1996.
4
Resistance to platelet microbicidal protein results in increased severity of experimental Candida albicans endocarditis.对血小板杀菌蛋白的抗性导致实验性白色念珠菌心内膜炎的严重程度增加。
Infect Immun. 1996 Apr;64(4):1379-84. doi: 10.1128/iai.64.4.1379-1384.1996.
5
Thrombin-induced rabbit platelet microbicidal protein is fungicidal in vitro.凝血酶诱导的兔血小板杀菌蛋白在体外具有杀真菌作用。
Antimicrob Agents Chemother. 1993 Mar;37(3):546-53. doi: 10.1128/AAC.37.3.546.
6
Effect of thrombocytopenia on the early course of streptococcal endocarditis.血小板减少对链球菌性心内膜炎早期病程的影响。
J Infect Dis. 1993 Oct;168(4):910-4. doi: 10.1093/infdis/168.4.910.
7
Role of the sar locus of Staphylococcus aureus in induction of endocarditis in rabbits.金黄色葡萄球菌sar基因座在兔心内膜炎诱导中的作用。
Infect Immun. 1994 May;62(5):1719-25. doi: 10.1128/iai.62.5.1719-1725.1994.
8
Platelet microbicidal protein alone and in combination with antibiotics reduces Staphylococcus aureus adherence to platelets in vitro.血小板杀菌蛋白单独使用以及与抗生素联合使用时，均可在体外减少金黄色葡萄球菌对血小板的黏附。
Infect Immun. 1994 Aug;62(8):3416-23. doi: 10.1128/iai.62.8.3416-3423.1994.
9
In vitro resistance to platelet microbicidal protein correlates with endocarditis source among bacteremic staphylococcal and streptococcal isolates.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。
Antimicrob Agents Chemother. 1994 Apr;38(4):729-32. doi: 10.1128/AAC.38.4.729.
10
Diminished virulence of a sar-/agr- mutant of Staphylococcus aureus in the rabbit model of endocarditis.金黄色葡萄球菌sar-/agr-突变体在兔心内膜炎模型中的毒力减弱。
J Clin Invest. 1994 Nov;94(5):1815-22. doi: 10.1172/JCI117530.