Hydrogen peroxide release by bacteria suppresses inflammasome-dependent innate immunity

被引:111
作者
Erttmann, Saskia F. [1 ]
Gekara, Nelson O. [1 ,2 ]
机构
[1] Umea Univ, UCMR, Lab Mol Infect Med Sweden MIMS, S-90187 Umea, Sweden
[2] Stockholm Univ, Dept Mol Biosci, Wenner Gren Inst, S-10691 Stockholm, Sweden
基金
瑞典研究理事会;
关键词
STREPTOCOCCUS-PNEUMONIAE; REACTIVE OXYGEN; NLRP3; INFLAMMASOME; OXIDATIVE STRESS; PYRUVATE OXIDASE; ACTIVATION; PROTEIN; CASPASE-1; PNEUMOLYSIN; VIRULENCE;
D O I
10.1038/s41467-019-11169-x
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];
摘要
Hydrogen peroxide (H2O2) has a major function in host-microbial interactions. Although most studies have focused on the endogenous H2O2 produced by immune cells to kill microbes, bacteria can also produce H2O2. How microbial H2O2 influences the dynamics of host-microbial interactions is unclear. Here we show that H2O2 released by Streptococcus pneumoniae inhibits inflammasomes, key components of the innate immune system, contributing to the pathogen colonization of the host. We also show that the oral commensal H2O2-producing bacteria Streptococcus oralis can block inflammasome activation. This study uncovers an unexpected role of H2O2 in immune suppression and demonstrates how, through this mechanism, bacteria might restrain the immune system to co-exist with the host.
引用
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页数:13
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