The cytochrome bd-I respiratory oxidase augments survival of multidrug-resistant Escherichia coli during infection

Shepherd, Mark, Achard, Maud E. S., Idris, Adi, Totsika, Makrina, Phan, Minh-Duy, Peters, Kate M., Sarkar, Sohinee, Ribeiro, Cláudia A., Holyoake, Louise V., Ladakis, Dimitrios, Ulett, Glen C., Sweet, Matthew J., Poole, Robert K., McEwan, Alastair G. and Schembri, Mark A. (2016) The cytochrome bd-I respiratory oxidase augments survival of multidrug-resistant Escherichia coli during infection. Scientific Reports, 6 . doi:10.1038/srep35285


Author Shepherd, Mark
Achard, Maud E. S.
Idris, Adi
Totsika, Makrina
Phan, Minh-Duy
Peters, Kate M.
Sarkar, Sohinee
Ribeiro, Cláudia A.
Holyoake, Louise V.
Ladakis, Dimitrios
Ulett, Glen C.
Sweet, Matthew J.
Poole, Robert K.
McEwan, Alastair G.
Schembri, Mark A.
Title The cytochrome bd-I respiratory oxidase augments survival of multidrug-resistant Escherichia coli during infection
Formatted title
The cytochrome bd-I respiratory oxidase augments survival of multidrug-resistant Escherichia coli during infection
Journal name Scientific Reports   Check publisher's open access policy
ISSN 2045-2322
Publication date 2016-10-21
Sub-type Article (original research)
DOI 10.1038/srep35285
Open Access Status DOI
Volume 6
Total pages 10
Place of publication London, United Kingdom
Publisher Nature Publishing Group
Language eng
Formatted abstract
Nitric oxide (NO) is a toxic free radical produced by neutrophils and macrophages in response to infection. Uropathogenic Escherichia coli (UPEC) induces a variety of defence mechanisms in response to NO, including direct NO detoxification (Hmp, NorVW, NrfA), iron-sulphur cluster repair (YtfE), and the expression of the NO-tolerant cytochrome bd-I respiratory oxidase (CydAB). The current study quantifies the relative contribution of these systems to UPEC growth and survival during infection. Loss of the flavohemoglobin Hmp and cytochrome bd-I elicit the greatest sensitivity to NO-mediated growth inhibition, whereas all but the periplasmic nitrite reductase NrfA provide protection against neutrophil killing and promote survival within activated macrophages. Intriguingly, the cytochrome bd-I respiratory oxidase was the only system that augmented UPEC survival in a mouse model after 2 days, suggesting that maintaining aerobic respiration under conditions of nitrosative stress is a key factor for host colonisation. These findings suggest that while UPEC have acquired a host of specialized mechanisms to evade nitrosative stresses, the cytochrome bd-I respiratory oxidase is the main contributor to NO tolerance and host colonisation under microaerobic conditions. This respiratory complex is therefore of major importance for the accumulation of high bacterial loads during infection of the urinary tract.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: HERDC Pre-Audit
School of Chemistry and Molecular Biosciences
Institute for Molecular Bioscience - Publications
 
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