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Spr1875 蛋白赋予了对肺炎链球菌引发的小胶质细胞杀伤的抗性。

The Spr1875 protein confers resistance to the microglia-mediated killing of Streptococcus pneumoniae.

机构信息

Dipartimento di Medicina Diagnostica, Clinica e di Sanità Pubblica, Università di Modena e Reggio Emilia (Unimore), 41125 Modena, Italy.

出版信息

Microb Pathog. 2013 Jun-Jul;59-60:42-7. doi: 10.1016/j.micpath.2013.04.002. Epub 2013 Apr 13.

Abstract

By screening a whole-genome λ-display library of Streptococcus pneumoniae, we have previously identified a novel surface protein, named Spr1875, that exhibited immunogenic properties and was closely related to pneumococcal virulence. In the present study, we investigated the role of the Spr1875 antigen in the interaction of S. pneumoniae with microglia, the resident brain macrophages. By using an in vitro infection model, the BV2 microglial cell line was challenged with the S. pneumoniae strain DP1004 and its isogenic spr1875-deleted mutant (Δspr1875). Both strains were phagocytosed by microglia efficiently and to a similar extent; however, the DP1004 strain was more resistant than the Δspr1875 mutant to the intracellular killing, as assessed by antibiotic protection and phagosome maturation assays. Moreover, significant differences between the two strains were also observed in terms of susceptibility to microglia-mediated killing. Taken together, these results indicate that S. pneumoniae-microglial cell interplay is influenced by the presence of Spr1875, suggesting that this protein may play a role in the pathogenesis of pneumococcal meningitis.

摘要

通过对肺炎链球菌全基因组 λ 展示文库进行筛选,我们先前鉴定出一种新型表面蛋白,命名为 Spr1875,该蛋白具有免疫原性,与肺炎链球菌的毒力密切相关。在本研究中,我们研究了 Spr1875 抗原在肺炎链球菌与脑内常驻巨噬细胞小神经胶质细胞相互作用中的作用。通过使用体外感染模型,用肺炎链球菌 DP1004 株及其同源缺失突变株(Δspr1875)感染 BV2 小神经胶质细胞系。两种菌株均被小神经胶质细胞有效吞噬,且吞噬程度相似;然而,与Δspr1875 突变株相比,DP1004 株对细胞内杀伤的抵抗力更强,这通过抗生素保护和吞噬体成熟测定来评估。此外,两种菌株在易感性方面也存在显著差异,小神经胶质细胞介导的杀伤。综上所述,这些结果表明肺炎链球菌-小神经胶质细胞相互作用受 Spr1875 的影响,提示该蛋白可能在肺炎球菌性脑膜炎的发病机制中发挥作用。

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