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首页> 外文期刊>Infection and immunity >Resistance to platelet microbicidal protein results in increased severity of experimental Candida albicans endocarditis.
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Resistance to platelet microbicidal protein results in increased severity of experimental Candida albicans endocarditis.

机译：对血小板杀微生物蛋白的抗性导致实验性白色念珠菌心内膜炎的严重性增加。

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Thrombin-induced platelet microbicidal protein (tPMP) exerts potent in vitro microbicidal activity against pathogens commonly found in the bloodstream, including Staphylococcus aureus, Staphylococcus epidermidis, and Candida albicans. Localized platelet release of tPMP may be important in defense against infections involving the vascular endothelium caused by tPMP-susceptible organisms. In contrast, pathogens capable of surviving in the presence of tPMP could then exploit the platelet as an adhesive surface for attachment to damaged endothelium. To examine these hypotheses, we derived a tPMP-resistant (tPMP(r)) C. albicans strain from its tPMP-sensitive (tPMP(s)) parental strains were equivalent in vitro as assessed by genotyping (electrophoretic karyotype and restriction endonuclease analysis of genomic DNA), biotyping, germination, platelet aggregation, adherence to vascular endothelial cells, and growth characteristics. In addition, the tPMP(r) phenotype was stable following multiple in vitro and in vivo passages. We then investigated the in vivo relevance of tPMP susceptibility on endovascular infection using a rabbit model of endocarditis and hematogenous dissemination. Rabbits with transaortic catheters (n = 15 in each group) were challenged with either the tPMP(s) or tPMP(r) C. albicans strain. All rabbits developed C. albicans-induced endocarditis, as determined by the presence of infected vegetations. In rabbits challenged with tPMP(s) strain (P < 0.001). These results were seen in the absence of differences in either initial adherence of strains to cardiac valves or vegetation weights. Furthermore, although these C. albicans strains induced equivalent rates and extent of hematogenous renal infection, only the tPMP(r) strain disseminated hematogenously to the spleen (15 of 15 rabbits) versus 0 of 15 [tpmp(s) strain]; P < 0.0001). Thus, tPMP(r) C. albicans caused more-severe endocarditis and produced greater metastatic sequelae than the tPMP(s) counterpart.
机译：凝血酶诱导的血小板杀微生物蛋白（tPMP）对血液中常见的病原体（包括金黄色葡萄球菌，表皮葡萄球菌和白色念珠菌）具有强大的体外杀微生物活性。 tPMP的局部血小板释放对于防御由tPMP易感生物引起的涉及血管内皮的感染可能很重要。相反，能够在tPMP存在下存活的病原体可以利用血小板作为附着在受损内皮上的粘附表面。为了检查这些假设，我们从其tPMP敏感（tPMP（s））亲本菌株衍生出了tPMP耐药（tPMP（r））的白色念珠菌菌株，通过基因分型（电泳核型和限制性核酸内切酶分析）评估了该菌株在体外是等效的。基因组DNA），生物分型，萌发，血小板聚集，对血管内皮细胞的粘附以及生长特性。另外，在多次体外和体内传代后，tPMP（r）表型稳定。然后，我们使用心内膜炎和血源性传播的兔子模型调查了tPMP敏感性对血管内感染的体内相关性。使用tPMP（s）或tPMP（r）白色念珠菌菌株对带有主动脉导管的兔子（每组n = 15）进行攻击。通过感染植物的存在来确定所有兔子都患有白色念珠菌诱导的心内膜炎。在用tPMP（s）菌株攻击的兔子中（P <0.001）。在菌株最初对心脏瓣膜的依从性或植物重量没有差异的情况下，可以看到这些结果。此外，尽管这些白色念珠菌菌株诱导的血源性肾脏感染率和程度相同，但只有tPMP（r）血源性地向脾脏扩散（15只兔中的15只），而15只中有0只[tpmp（s）]。 P <0.0001）。因此，tPMP（r）白色念珠菌引起的心内膜炎比tPMP更为严重，并产生更大的转移性后遗症。

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