Recognition of Streptococcus pneumoniae by the innate immune system

被引:145
|
作者
Koppe, Uwe [1 ]
Suttorp, Norbert [1 ]
Opitz, Bastian [1 ]
机构
[1] Charite Univ Med Berlin, Dept Internal Med Infect Dis & Pulm Med, D-13353 Berlin, Germany
关键词
IMPAIRED HOST-DEFENSE; TOLL-LIKE RECEPTOR-4; PNEUMOCOCCAL PNEUMONIA; DEFICIENT MICE; NLRP3; INFLAMMASOME; VIRULENCE FACTORS; LUNG INJURY; PNEUMOLYSIN; TOLL-LIKE-RECEPTOR-2; COLONIZATION;
D O I
10.1111/j.1462-5822.2011.01746.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Streptococcus pneumoniae is both a frequent colonizer of the upper respiratory tract and a leading cause of life-threatening infections such as pneumonia, meningitis and sepsis. The innate immune system is critical for the control of colonization and for defence during invasive disease. Initially, pneumococci are recognized by different sensors of the innate immune system called pattern recognition receptors (PRRs), which control most subsequent host defence pathways. These PRRs include the transmembrane Toll-like receptors (TLRs) as well as the cytosolic NOD-like receptors (NLRs) and DNA sensors. Recognition of S. pneumoniae by members of these PRR families regulates the production of inflammatory mediators that orchestrate the following immune response of infected as well as neighbouring non-infected cells, stimulates the recruitment of immune cells such as neutrophils and macrophages, and shapes the adaptive immunity. This review summarizes the current knowledge of the function of different PRRs in S. pneumoniae infection.
引用
收藏
页码:460 / 466
页数:7
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