Cytochrome bd promotes Escherichia coli biofilm antibiotic tolerance by regulating accumulation of noxious chemicals.


Journal

NPJ biofilms and microbiomes
ISSN: 2055-5008
Titre abrégé: NPJ Biofilms Microbiomes
Pays: United States
ID NLM: 101666944

Informations de publication

Date de publication:
16 04 2021
Historique:
received: 16 11 2020
accepted: 16 03 2021
entrez: 17 4 2021
pubmed: 18 4 2021
medline: 11 8 2021
Statut: epublish

Résumé

Nutrient gradients in biofilms cause bacteria to organize into metabolically versatile communities capable of withstanding threats from external agents including bacteriophages, phagocytes, and antibiotics. We previously determined that oxygen availability spatially organizes respiration in uropathogenic Escherichia coli biofilms, and that the high-affinity respiratory quinol oxidase cytochrome bd is necessary for extracellular matrix production and biofilm development. In this study we investigate the physiologic consequences of cytochrome bd deficiency in biofilms and determine that loss of cytochrome bd induces a biofilm-specific increase in expression of general diffusion porins, leading to elevated outer membrane permeability. In addition, loss of cytochrome bd impedes the proton mediated efflux of noxious chemicals by diminishing respiratory flux. As a result, loss of cytochrome bd enhances cellular accumulation of noxious chemicals and increases biofilm susceptibility to antibiotics. These results identify an undescribed link between E. coli biofilm respiration and stress tolerance, while suggesting the possibility of inhibiting cytochrome bd as an antibiofilm therapeutic approach.

Identifiants

pubmed: 33863914
doi: 10.1038/s41522-021-00210-x
pii: 10.1038/s41522-021-00210-x
pmc: PMC8052454
doi:

Substances chimiques

Anti-Bacterial Agents 0
Bacterial Outer Membrane Proteins 0
Cytochrome b Group 0
Electron Transport Chain Complex Proteins 0
Escherichia coli Proteins 0
Oxidoreductases EC 1.-
cytochrome bd terminal oxidase complex, E coli EC 1.9.3.-

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

35

Subventions

Organisme : NIAID NIH HHS
ID : F30 AI150077
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM007347
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI107052
Pays : United States
Organisme : NIDDK NIH HHS
ID : P20 DK123967
Pays : United States

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Auteurs

Connor J Beebout (CJ)

Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA.

Levy A Sominsky (LA)

Vanderbilt University, Nashville, TN, USA.

Allison R Eberly (AR)

Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA.
Division of Clinical Microbiology, Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA.

Gerald T Van Horn (GT)

Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA.

Maria Hadjifrangiskou (M)

Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA. maria.hadjifrangiskou@vumc.org.
Vanderbilt Institute for Infection, Immunology, and Inflammation, Vanderbilt University Medical Center, Nashville, TN, USA. maria.hadjifrangiskou@vumc.org.

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