Role of complement in host-microbe homeostasis of the periodontium

被引：62

作者：

Hajishengallis, George ^{[1
]}

Abe, Toshiharu ^{[1
]}

Maekawa, Tomoki ^{[1
]}

Hajishengallis, Evlambia ^{[2
]}

Lambris, John D. ^{[3
]}

机构：

[1] Univ Penn, Sch Dent Med, Dept Microbiol, Philadelphia, PA 19104 USA

[2] Univ Penn, Sch Dent Med, Dept Restorat & Prevent Sci, Philadelphia, PA 19104 USA

[3] Univ Penn, Sch Dent Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA

来源：

SEMINARS IN IMMUNOLOGY | 2013年 / 25卷 / 01期

基金：

美国国家卫生研究院;

关键词：

Complement; C5a receptor; Periodontitis; Dysbiosis; Porphyromonas gingivalis; GINGIVAL CREVICULAR FLUID; PORPHYROMONAS-GINGIVALIS; ACTINOBACILLUS-ACTINOMYCETEMCOMITANS; PREVOTELLA-INTERMEDIA; CYSTEINE PROTEINASES; CLEAVAGE PRODUCTS; GENE-EXPRESSION; COMPONENTS C3; ACTIVATION; HEALTH;

D O I：

10.1016/j.smim.2013.04.004

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Complement plays a key role in immunity and inflammation through direct effects on immune cells or via crosstalk and regulation of other host signaling pathways. Deregulation of these finely balanced complement activities can link infection to inflammatory tissue damage. Periodontitis is a polymicrobial community-induced chronic inflammatory disease that can destroy the tooth-supporting tissues. In this review, we summarize and discuss evidence that complement is involved in the dysbiotic transformation of the periodontal microbiota and in the inflammatory process that leads to the destruction of periodontal bone. Recent insights into the mechanisms of complement involvement in periodontitis have additionally provided likely targets for therapeutic intervention against this oral disease. (C) 2013 Elsevier Ltd. All rights reserved.

引用

页码：65 / 72

页数：8

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