Lipoprotein signal peptidase-deficient Streptococcus pneumoniae exhibits impaired Toll-like receptor 2-stimulatory activity

IF 1.9 4区 医学 Q4 IMMUNOLOGY
Hisanori Domon, Satoru Hirayama, Toshihito Isono, Rui Saito, Katsunori Yanagihara, Yutaka Terao
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引用次数: 0

Abstract

Streptococcus pneumoniae is a causative agent of community-acquired pneumonia. Upon pneumococcal infection, innate immune cells recognize pneumococcal lipoproteins via Toll-like receptor 2 and induce inflammation. Here, we generated a strain of S. pneumoniae deficient in lipoprotein signal peptidase (LspA), a transmembrane type II signal peptidase required for lipoprotein maturation, to investigate the host immune response against this strain. Triton X-114 phase separation revealed that lipoprotein expression was lower in the LspA-deficient strain than in the wild-type strain. Additionally, the LspA-deficient strain decreased nuclear factor-κB activation and cytokine production in THP-1 cells, indicating impaired innate immune response against the strain.

脂蛋白信号肽酶缺陷的肺炎链球菌表现出受损的 Toll 样受体 2 刺激活性。
肺炎链球菌是社区获得性肺炎的致病菌。感染肺炎球菌后,先天性免疫细胞会通过 Toll 样受体 2 识别肺炎球菌脂蛋白并诱发炎症。在这里,我们生成了一株缺乏脂蛋白信号肽酶(LspA)的肺炎球菌,以研究宿主对该菌株的免疫反应。Triton X-114 相分离显示,LspA 缺陷菌株的脂蛋白表达量低于野生型菌株。此外,LspA缺陷株降低了THP-1细胞中核因子-κB的活化和细胞因子的产生,表明针对该菌株的先天免疫反应受损。
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来源期刊
Microbiology and Immunology
Microbiology and Immunology 医学-免疫学
CiteScore
5.20
自引率
3.80%
发文量
78
审稿时长
1 months
期刊介绍: Microbiology and Immunology is published in association with Japanese Society for Bacteriology, Japanese Society for Virology, and Japanese Society for Host Defense Research. It is peer-reviewed publication that provides insight into the study of microbes and the host immune, biological and physiological responses. Fields covered by Microbiology and Immunology include:Bacteriology|Virology|Immunology|pathogenic infections in human, animals and plants|pathogenicity and virulence factors such as microbial toxins and cell-surface components|factors involved in host defense, inflammation, development of vaccines|antimicrobial agents and drug resistance of microbes|genomics and proteomics.
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