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生物膜的形成可以避免肺炎链球菌被补体免疫和吞噬作用清除。

Biofilm formation avoids complement immunity and phagocytosis of Streptococcus pneumoniae.

机构信息

Department of Molecular Microbiology and Infection Biology, Centro de Investigaciones Biológicas, Madrid, Spain.

出版信息

Infect Immun. 2013 Jul;81(7):2606-15. doi: 10.1128/IAI.00491-13. Epub 2013 May 6.

Abstract

Streptococcus pneumoniae is a frequent member of the microbiota of the human nasopharynx. Colonization of the nasopharyngeal tract is a first and necessary step in the infectious process and often involves the formation of sessile microbial communities by this human pathogen. The ability to grow and persist as biofilms is an advantage for many microorganisms, because biofilm-grown bacteria show reduced susceptibility to antimicrobial agents and hinder recognition by the immune system. The extent of host protection against biofilm-related pneumococcal disease has not been determined yet. Using pneumococcal strains growing as planktonic cultures or as biofilms, we have investigated the recognition of S. pneumoniae by the complement system and its interactions with human neutrophils. Deposition of C3b, the key complement component, was impaired on S. pneumoniae biofilms. In addition, binding of C-reactive protein and the complement component C1q to the pneumococcal surface was reduced in biofilm bacteria, demonstrating that pneumococcal biofilms avoid the activation of the classical complement pathway. In addition, recruitment of factor H, the downregulator of the alternative pathway, was enhanced by S. pneumoniae growing as biofilms. Our results also show that biofilm formation diverts the alternative complement pathway activation by a PspC-mediated mechanism. Furthermore, phagocytosis of pneumococcal biofilms was also impaired. The present study confirms that biofilm formation in S. pneumoniae is an efficient means of evading both the classical and the PspC-dependent alternative complement pathways the host immune system.

摘要

肺炎链球菌是人类鼻咽部微生物群的常见成员。鼻咽部定植是感染过程的第一步也是必要条件,通常涉及这种人类病原体形成固定的微生物群落。作为生物膜生长的能力是许多微生物的优势,因为生物膜生长的细菌对抗生素的敏感性降低,并阻碍免疫系统的识别。宿主对生物膜相关肺炎球菌病的保护程度尚未确定。使用作为浮游培养物或生物膜生长的肺炎链球菌菌株,我们研究了补体系统对肺炎链球菌的识别及其与人类中性粒细胞的相互作用。C3b 的沉积,关键的补体成分,在肺炎链球菌生物膜上受损。此外,C 反应蛋白和补体成分 C1q 与肺炎链球菌表面的结合在生物膜细菌中减少,表明肺炎链球菌生物膜避免了经典补体途径的激活。此外,生长为生物膜的肺炎链球菌增强了因子 H 的募集,因子 H 是替代途径的下调因子。我们的结果还表明,生物膜形成通过 PspC 介导的机制改变替代补体途径的激活。此外,肺炎链球菌生物膜的吞噬作用也受损。本研究证实,肺炎链球菌生物膜的形成是逃避宿主免疫系统的经典和 PspC 依赖性替代补体途径的有效手段。

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