Dhawan V K, Bayer A S, Yeaman M R
Charles Drew University-Martin Luther King Medical Center, Los Angeles, California 90059, USA.
Infect Immun. 1998 Jul;66(7):3476-9. doi: 10.1128/IAI.66.7.3476-3479.1998.
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.
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。