期刊
JOURNAL OF INNATE IMMUNITY
卷 6, 期 2, 页码 240-250出版社
KARGER
DOI: 10.1159/000353754
关键词
Complement; Innate immunity; M protein; Phagocytosis; Plasmin(ogen); Streptococcus pyogenes
类别
资金
- Australian Postgraduate Award
- NHMRC (National Health and Medical Research Council) Career Development Fellowship
- NHMRC [635218]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI077780] Funding Source: NIH RePORTER
The globally significant human pathogen group A Streptococcus (GAS) sequesters the host protease plasmin to the cell surface during invasive disease initiation. Recent evidence has shown that localized plasmin activity prevents opsonization of several bacterial species by key components of the innate immune system in vitro. Here we demonstrate that plasmin at the GAS cell surface resulted in degradation of complement factor C3b, and that plasminogen acquisition is associated with a decrease in C3b opsonization and neutrophil-mediated killing in vitro. Furthermore, the ability to acquire cell surface plasmin(ogen) correlates directly with a decrease in C3b opsonization, neutrophil phagocytosis, and increased bacterial survival in a humanized plasminogen mouse model of infection. These findings demonstrate that localized plasmin(ogen) plays an important role in facilitating GAS escape from the host innate immune response and increases bacterial virulence in the early stages of infection. Copyright (C) 2013 S. Karger AG, Basel
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据