O2-inducible H2O2-forming NADPH oxidase is responsible for the hyper O2 sensitivity of Bifidobacterium longum subsp. infantis

Abstract Bifidobacteria are beneficial anaerobes, and their O2 sensitivity levels differ among species as a function of unknown molecular mechanisms. Bifidobacterium longum subspecies infantis (B. infantis), a predominant colonizer of the gastrointestinal tract of infants, showed a hyper O2-sensitiv...

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Main Authors: Kunifusa Tanaka, Takumi Satoh, Jun Kitahara, Saori Uno, Izumi Nomura, Yasunobu Kano, Tohru Suzuki, Youichi Niimura, Shinji Kawasaki
Format: Article
Language:English
Published: Nature Portfolio 2018-07-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-018-29030-4
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author Kunifusa Tanaka
Takumi Satoh
Jun Kitahara
Saori Uno
Izumi Nomura
Yasunobu Kano
Tohru Suzuki
Youichi Niimura
Shinji Kawasaki
author_facet Kunifusa Tanaka
Takumi Satoh
Jun Kitahara
Saori Uno
Izumi Nomura
Yasunobu Kano
Tohru Suzuki
Youichi Niimura
Shinji Kawasaki
author_sort Kunifusa Tanaka
collection DOAJ
description Abstract Bifidobacteria are beneficial anaerobes, and their O2 sensitivity levels differ among species as a function of unknown molecular mechanisms. Bifidobacterium longum subspecies infantis (B. infantis), a predominant colonizer of the gastrointestinal tract of infants, showed a hyper O2-sensitive growth profile with accompanying a production of H2O2. In this study, we characterized an NADPH oxidase as a key enzyme responsible for this microbe’s hyper O2 sensitivity. A dominant active elution peak of H2O2-forming NADPH oxidase activity was detected in the first step of column chromatography, and the purified NADPH oxidase (NPOX) was identified as a homolog of nitroreductase family proteins. The introduction of the gene encoding B. infantis NPOX (npoxA) into O2-tolerant Bifidobacterium minimum made the strain O2 sensitive and allowed it to produce H2O2. Knockout of the npoxA gene in B. infantis decreased the production of H2O2 and mitigated its B. infantis hyper O2 sensitivity. A transcript of B. infantis npoxA is induced by O2, suggesting that the aerobic production of toxic H2O2 is functionally conserved in B. infantis.
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spelling doaj.art-370bf879625949e88502e25b7c015e9d2022-12-21T22:54:26ZengNature PortfolioScientific Reports2045-23222018-07-018111010.1038/s41598-018-29030-4O2-inducible H2O2-forming NADPH oxidase is responsible for the hyper O2 sensitivity of Bifidobacterium longum subsp. infantisKunifusa Tanaka0Takumi Satoh1Jun Kitahara2Saori Uno3Izumi Nomura4Yasunobu Kano5Tohru Suzuki6Youichi Niimura7Shinji Kawasaki8Department of Bioscience, Tokyo University of AgricultureDepartment of Molecular Microbiology, Tokyo University of AgricultureDepartment of Bioscience, Tokyo University of AgricultureDepartment of Bioscience, Tokyo University of AgricultureFaculty of Applied Biological Sciences, Gifu UniversityDepartment of Molecular Genetics, Kyoto Pharmaceutical UniversityFaculty of Applied Biological Sciences, Gifu UniversityDepartment of Molecular Microbiology, Tokyo University of AgricultureDepartment of Molecular Microbiology, Tokyo University of AgricultureAbstract Bifidobacteria are beneficial anaerobes, and their O2 sensitivity levels differ among species as a function of unknown molecular mechanisms. Bifidobacterium longum subspecies infantis (B. infantis), a predominant colonizer of the gastrointestinal tract of infants, showed a hyper O2-sensitive growth profile with accompanying a production of H2O2. In this study, we characterized an NADPH oxidase as a key enzyme responsible for this microbe’s hyper O2 sensitivity. A dominant active elution peak of H2O2-forming NADPH oxidase activity was detected in the first step of column chromatography, and the purified NADPH oxidase (NPOX) was identified as a homolog of nitroreductase family proteins. The introduction of the gene encoding B. infantis NPOX (npoxA) into O2-tolerant Bifidobacterium minimum made the strain O2 sensitive and allowed it to produce H2O2. Knockout of the npoxA gene in B. infantis decreased the production of H2O2 and mitigated its B. infantis hyper O2 sensitivity. A transcript of B. infantis npoxA is induced by O2, suggesting that the aerobic production of toxic H2O2 is functionally conserved in B. infantis.https://doi.org/10.1038/s41598-018-29030-4
spellingShingle Kunifusa Tanaka
Takumi Satoh
Jun Kitahara
Saori Uno
Izumi Nomura
Yasunobu Kano
Tohru Suzuki
Youichi Niimura
Shinji Kawasaki
O2-inducible H2O2-forming NADPH oxidase is responsible for the hyper O2 sensitivity of Bifidobacterium longum subsp. infantis
Scientific Reports
title O2-inducible H2O2-forming NADPH oxidase is responsible for the hyper O2 sensitivity of Bifidobacterium longum subsp. infantis
title_full O2-inducible H2O2-forming NADPH oxidase is responsible for the hyper O2 sensitivity of Bifidobacterium longum subsp. infantis
title_fullStr O2-inducible H2O2-forming NADPH oxidase is responsible for the hyper O2 sensitivity of Bifidobacterium longum subsp. infantis
title_full_unstemmed O2-inducible H2O2-forming NADPH oxidase is responsible for the hyper O2 sensitivity of Bifidobacterium longum subsp. infantis
title_short O2-inducible H2O2-forming NADPH oxidase is responsible for the hyper O2 sensitivity of Bifidobacterium longum subsp. infantis
title_sort o2 inducible h2o2 forming nadph oxidase is responsible for the hyper o2 sensitivity of bifidobacterium longum subsp infantis
url https://doi.org/10.1038/s41598-018-29030-4
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