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革兰阳性病原体对补体的抑制：分子机制及治疗意义。

Complement inhibition by gram-positive pathogens: molecular mechanisms and therapeutic implications.

机构信息

Medical Microbiology, University Medical Center Utrecht, PO G04.614, Heidelberglaan 100, 3584 CX Utrecht, the Netherlands.

出版信息

J Mol Med (Berl). 2010 Feb;88(2):115-20. doi: 10.1007/s00109-009-0572-y.

DOI:10.1007/s00109-009-0572-y
PMID:20062962
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2832872/
Abstract

The plasma proteins of the complement system are essential in the innate immune response against bacteria. Complement labels bacteria with opsonins to support phagocytosis and generates chemoattractants to attract phagocytes to the site of infection. In turn, bacterial human pathogens have evolved different strategies to specifically impair the complement response. Here, we review the large arsenal of complement inhibitors produced by the gram-positive pathogens Staphylococcus aureus and Group A Streptococcus. We discuss how these bacterial molecules provide us with new tools to treat both infectious and inflammatory disease conditions in humans.

摘要

补体系统的血浆蛋白在针对细菌的先天免疫反应中至关重要。补体通过调理素标记细菌，以支持吞噬作用，并产生趋化因子吸引吞噬细胞到感染部位。反过来，细菌病原体已经进化出不同的策略来特异性地削弱补体反应。在这里，我们回顾了革兰氏阳性病原体金黄色葡萄球菌和 A 组链球菌产生的大量补体抑制剂。我们讨论了这些细菌分子如何为我们提供新的工具来治疗人类的感染和炎症性疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3ad/2832872/4745be8db100/109_2009_572_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3ad/2832872/c098d5e313cc/109_2009_572_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3ad/2832872/c441e1418a65/109_2009_572_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3ad/2832872/4745be8db100/109_2009_572_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3ad/2832872/c098d5e313cc/109_2009_572_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3ad/2832872/c441e1418a65/109_2009_572_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e3ad/2832872/4745be8db100/109_2009_572_Fig3_HTML.jpg

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Complement inhibition by gram-positive pathogens: molecular mechanisms and therapeutic implications.

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本文引用的文献

[1]
A molecular insight into complement evasion by the staphylococcal complement inhibitor protein family.

J Immunol. 2009-8-15

[2]
Structural and functional implications of the alternative complement pathway C3 convertase stabilized by a staphylococcal inhibitor.

Nat Immunol. 2009-7

[3]
Complement evasion strategies of pathogens-acquisition of inhibitors and beyond.

Mol Immunol. 2009-9

[4]
Structure of the tyrosine-sulfated C5a receptor N terminus in complex with chemotaxis inhibitory protein of Staphylococcus aureus.

J Biol Chem. 2009-5-1

[5]
Complement activation and inhibition: a delicate balance.

Trends Immunol. 2009-2

[6]
The Staphylococcus aureus protein Sbi acts as a complement inhibitor and forms a tripartite complex with host complement Factor H and C3b.

PLoS Pathog. 2008-12

[7]
Staphylococcal complement inhibitors: biological functions, recognition of complement components, and potential therapeutic implications.

Adv Exp Med Biol. 2008

[8]
Cutting edge: members of the Staphylococcus aureus extracellular fibrinogen-binding protein family inhibit the interaction of C3d with complement receptor 2.

J Immunol. 2008-12-1

[9]
Staphylococcus aureus clumping factor A binds to complement regulator factor I and increases factor I cleavage of C3b.

J Infect Dis. 2008-7-1

[10]
Interaction of human complement with Sbi, a staphylococcal immunoglobulin-binding protein: indications of a novel mechanism of complement evasion by Staphylococcus aureus.

J Biol Chem. 2008-6-20

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