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首页> 外文期刊>Infection and immunity >Glucosyltransferases of Viridans Streptococci Are Modulins of Interleukin-6 Induction in Infective Endocarditis
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Glucosyltransferases of Viridans Streptococci Are Modulins of Interleukin-6 Induction in Infective Endocarditis

机译：Viridans Streptococci的葡萄糖转移酶是感染性心内膜炎中白细胞介素-6诱导的调节剂

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The glucosyltransferases (GTFs) of viridans streptococci, common pathogens of infective endocarditis, are extracellular proteins that convert sucrose into exopolysaccharides and glucans. GTFs B, C, and D of Streptococcus mutans are modulins that induce, in vitro and in vivo, the production of cytokines, in particular interleukin-6 (IL-6), from monocytes. The roles of S. mutans GTFs in infectivity and inflammation in situ were tested in a rat experimental model of endocarditis. No significant differences in infectivity, in terms of 95% infective dose and densities of bacteria inside vegetations, were observed between laboratory strain GS-5 and two clinical isolates or isogenic mutant NHS1DD, defective in the expression of GTFs. In aortic valves and surrounding tissues, IL-6 was detected by Western blots and immunostaining 24 h after GS-5 infection, was maintained over 72 h, and was followed by production of tumor necrosis factor alpha but not IL-1β. Animals infected with NHS1DD showed markedly lower levels of IL-6 (less than 5% of that of parental GS-5-infected rats), while tumor necrosis factor alpha was unaffected. In contrast, animals infected with NHR1DD, another isogenic mutant expressing only GtfB, showed a much smaller reduction (down to 56%). These results suggest that GTFs are specific modulins that act during acute inflammation, inducing IL-6 from endothelial cells surrounding the infected valves without affecting bacterial colonization in vegetations, and that IL-6 might persist in chronic inflammation in endocarditis.
机译：Viridans Streptococci，感染性心内膜炎的常见病原体的葡萄糖转移酶（GTF）是将蔗糖转化为外核和葡聚糖的细胞外蛋白质。 GTFS B，C和D的链球菌Mutans 是诱导，体外和体内，细胞因子，特别是白细胞介素-6（IL-6）的调节蛋白，从单核细胞中产生细胞因子。 S的角色。在心内膜炎的大鼠实验模型中测试感染性和炎症中的变形性和炎症的GTFs。在实验室菌株GS-5和两种临床分离株或中源性突变体NHS1DD之间观察到植被内部的95％感染剂量和细菌的密度没有显着差异，从95％的感染剂量和植被内部的细菌密度。在主动脉瓣和周围组织中，通过Western印迹和GS-5感染后24小时检测IL-6，保持超过72小时，然后进行肿瘤坏死因子α但不是IL-1β。感染NHS1DD的动物表现出显着较低的IL-6水平（少于亲属GS-5感染大鼠的5％），而肿瘤坏死因子α不受影响。相比之下，感染NHR1DD的动物，仅表达GTFB的另一个同种型突变体，表现出更小的还原（低至56％）。这些结果表明，GTFS是在急性炎症期间作用的特异性调节蛋白，诱导来自感染阀周围的内皮细胞的IL-6，而不会影响植被中的细菌定植，并且IL-6可能持续在心内腔中的慢性炎症中。

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