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本文引用的文献

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Vancomycin tolerance in Gram-positive cocci.革兰阳性球菌的万古霉素耐药性。
Environ Microbiol Rep. 2011 Dec;3(6):640-50. doi: 10.1111/j.1758-2229.2011.00254.x. Epub 2011 Apr 20.
2
Human and pneumococcal cell surface glyceraldehyde-3-phosphate dehydrogenase (GAPDH) proteins are both ligands of human C1q protein.人源和肺炎球菌细胞表面甘油醛-3-磷酸脱氢酶(GAPDH)蛋白均为人 C1q 蛋白的配体。
J Biol Chem. 2012 Dec 14;287(51):42620-33. doi: 10.1074/jbc.M112.423731. Epub 2012 Oct 18.
3
Enolase of Streptococcus pneumoniae binds human complement inhibitor C4b-binding protein and contributes to complement evasion.肺炎链球菌烯醇化酶结合人补体抑制剂 C4b 结合蛋白并有助于补体逃避。
J Immunol. 2012 Oct 1;189(7):3575-84. doi: 10.4049/jimmunol.1102934. Epub 2012 Aug 27.
4
Insight into the composition of the intercellular matrix of Streptococcus pneumoniae biofilms.洞察肺炎链球菌生物膜细胞外基质的组成。
Environ Microbiol. 2013 Feb;15(2):502-16. doi: 10.1111/j.1462-2920.2012.02853.x. Epub 2012 Aug 23.
5
The lectin pathway of complement activation is a critical component of the innate immune response to pneumococcal infection.补体激活的凝集素途径是对肺炎球菌感染固有免疫反应的关键组成部分。
PLoS Pathog. 2012;8(7):e1002793. doi: 10.1371/journal.ppat.1002793. Epub 2012 Jul 5.
6
Streptococcus pneumoniae in biofilms are unable to cause invasive disease due to altered virulence determinant production.生物膜中的肺炎链球菌由于毒力决定因素的产生发生改变而无法引起侵袭性疾病。
PLoS One. 2011;6(12):e28738. doi: 10.1371/journal.pone.0028738. Epub 2011 Dec 8.
7
Biofilm and planktonic pneumococci demonstrate disparate immunoreactivity to human convalescent sera.生物膜和浮游状态肺炎球菌与人恢复期血清的免疫反应不同。
BMC Microbiol. 2011 Nov 2;11:245. doi: 10.1186/1471-2180-11-245.
8
Biofilm formation in Streptococcus pneumoniae.肺炎链球菌生物膜的形成。
Microb Biotechnol. 2012 Jul;5(4):455-65. doi: 10.1111/j.1751-7915.2011.00294.x. Epub 2011 Sep 9.
9
Nasopharyngeal colonization and invasive disease are enhanced by the cell wall hydrolases LytB and LytC of Streptococcus pneumoniae.肺炎链球菌细胞壁水解酶 LytB 和 LytC 增强鼻咽部定植和侵袭性疾病。
PLoS One. 2011;6(8):e23626. doi: 10.1371/journal.pone.0023626. Epub 2011 Aug 23.
10
Bacterial virulence in the moonlight: multitasking bacterial moonlighting proteins are virulence determinants in infectious disease.细菌在月光下的毒力:多功能细菌 moonlighting 蛋白是传染病中的毒力决定因素。
Infect Immun. 2011 Sep;79(9):3476-91. doi: 10.1128/IAI.00179-11. Epub 2011 Jun 6.

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.

DOI:10.1128/IAI.00491-13
PMID:23649097
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3697597/
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。