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Hydrogen peroxide release by bacteria suppresses inflammasome-dependent innate immunity
Umeå University, Faculty of Medicine, Umeå Centre for Microbial Research (UCMR). Umeå University, Faculty of Medicine, Molecular Infection Medicine Sweden (MIMS). (Erttmann)ORCID iD: 0000-0003-2398-8405
Umeå University, Faculty of Medicine, Molecular Infection Medicine Sweden (MIMS). Umeå University, Faculty of Medicine, Umeå Centre for Microbial Research (UCMR). Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.ORCID iD: 0000-0002-1269-8288
2019 (English)In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 10, article id 3493Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
Nature Publishing Group, 2019. Vol. 10, article id 3493
Keywords [en]
Inflammasome
National Category
Cell and Molecular Biology
Research subject
Immunology; cell research; Infectious Diseases
Identifiers
URN: urn:nbn:se:umu:diva-162589DOI: 10.1038/s41467-019-11169-xISI: 000478576800011PubMedID: 31375698OAI: oai:DiVA.org:umu-162589DiVA, id: diva2:1345165
Available from: 2019-08-23 Created: 2019-08-23 Last updated: 2019-08-30Bibliographically approved

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Erttmann, Saskia F.Gekara, Nelson O.

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