Nitric oxide-mediated induction of dispersal in pseudomonas aeruginosa biofilms is inhibited by flavohemoglobin production and is enhanced by imidazole

Zhu, X; Oh, HS; Ng, YCB; Tang, PYP; Barraud, N; Riceb, SA

Nitric oxide-mediated induction of dispersal in pseudomonas aeruginosa biofilms is inhibited by flavohemoglobin production and is enhanced by imidazole

Zhu, X Oh, HS Ng, YCB Tang, PYP Barraud, N Riceb, SA

Permalink

Publication Type:: Journal Article
Citation:: Antimicrobial Agents and Chemotherapy, 2018, 62 (3)
Issue Date:: 2018-03-01

Open Access

Copyright Clearance Process

Recently Added
In Progress
Open Access

This item is open access.

Adobe PDF

Download Accepted Manuscript VersionAdobe PDF (1.67 MB)

View on publisher's site

View statistics

Full metadata record

Field	Value	Language
dc.contributor.author	Zhu, X	en_US
dc.contributor.author	Oh, HS	en_US
dc.contributor.author	Ng, YCB	en_US
dc.contributor.author	Tang, PYP	en_US
dc.contributor.author	Barraud, N	en_US
dc.contributor.author	Riceb, SA https://orcid.org/0000-0002-9486-2343	en_US
dc.date.available	2020-05-25T19:11:38Z
dc.date.issued	2018-03-01	en_US
dc.identifier.citation	Antimicrobial Agents and Chemotherapy, 2018, 62 (3)	en_US
dc.identifier.issn	0066-4804	en_US
dc.identifier.uri	http://hdl.handle.net/10453/124082
dc.description.abstract	Copyright © 2018 American Society for Microbiology. All Rights Reserved. The biological signal molecule nitric oxide (NO) was found to induce biofilm dispersal across a range of bacterial species, which led to its consideration for therapeutic strategies to treat biofilms and biofilm-related infections. However, biofilms are often not completely dispersed after exposure to NO. To better understand this phenomenon, we investigated the response of Pseudomonas aeruginosa biofilm cells to successive NO treatments. When biofilms were first pretreated with a low, noneffective dose of NO, a second dose of the signal molecule at a concentration usually capable of inducing dispersal did not have any effect. Amperometric analysis revealed that pretreated P. aeruginosa cells had enhanced NO-scavenging activity, and this effect was associated with the production of the flavohemoglobin Fhp. Further, quantitative real-time reverse transcription-PCR (qRT-PCR) analysis showed that fhp expression increased by over 100-fold in NO-pretreated biofilms compared to untreated biofilms. Biofilms of mutant strains harboring mutations in fhp or fhpR, encoding a NO-responsive regulator of fhp, were not affected in their dispersal response after the initial pretreatment with NO. Overall, these results suggest that FhpR can sense NO to trigger production of the flavohemoglobin Fhp and inhibit subsequent dispersal responses to NO. Finally, the addition of imidazole, which can inhibit the NO dioxygenase activity of flavohemoglobin, attenuated the prevention of dispersal after NO pretreatment and improved the dispersal response in older, starved biofilms. This study clarifies the underlying mechanisms of impaired dispersal induced by repeated NO treatments and offers a new perspective for improving the use of NO in biofilm control strategies.	en_US
dc.relation.ispartof	Antimicrobial Agents and Chemotherapy	en_US
dc.relation.isbasedon	10.1128/AAC.01832-17	en_US
dc.subject.classification	Microbiology	en_US
dc.subject.mesh	Biofilms	en_US
dc.subject.mesh	Pseudomonas aeruginosa	en_US
dc.subject.mesh	Nitric Oxide	en_US
dc.subject.mesh	Imidazoles	en_US
dc.subject.mesh	Dihydropteridine Reductase	en_US
dc.subject.mesh	Bacterial Proteins	en_US
dc.subject.mesh	Gene Expression Regulation, Bacterial	en_US
dc.title	Nitric oxide-mediated induction of dispersal in pseudomonas aeruginosa biofilms is inhibited by flavohemoglobin production and is enhanced by imidazole	en_US
dc.type	Journal Article
utslib.citation.volume	3	en_US
utslib.citation.volume	62	en_US
utslib.for	0605 Microbiology	en_US
utslib.for	1108 Medical Microbiology	en_US
utslib.for	1115 Pharmacology and Pharmaceutical Sciences	en_US
pubs.embargo.period	Not known	en_US
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Strength - ithree - Institute of Infection, Immunity and Innovation
utslib.copyright.status	open_access
pubs.issue	3	en_US
pubs.publication-status	Published	en_US
pubs.volume	62	en_US

Abstract:

Copyright © 2018 American Society for Microbiology. All Rights Reserved. The biological signal molecule nitric oxide (NO) was found to induce biofilm dispersal across a range of bacterial species, which led to its consideration for therapeutic strategies to treat biofilms and biofilm-related infections. However, biofilms are often not completely dispersed after exposure to NO. To better understand this phenomenon, we investigated the response of Pseudomonas aeruginosa biofilm cells to successive NO treatments. When biofilms were first pretreated with a low, noneffective dose of NO, a second dose of the signal molecule at a concentration usually capable of inducing dispersal did not have any effect. Amperometric analysis revealed that pretreated P. aeruginosa cells had enhanced NO-scavenging activity, and this effect was associated with the production of the flavohemoglobin Fhp. Further, quantitative real-time reverse transcription-PCR (qRT-PCR) analysis showed that fhp expression increased by over 100-fold in NO-pretreated biofilms compared to untreated biofilms. Biofilms of mutant strains harboring mutations in fhp or fhpR, encoding a NO-responsive regulator of fhp, were not affected in their dispersal response after the initial pretreatment with NO. Overall, these results suggest that FhpR can sense NO to trigger production of the flavohemoglobin Fhp and inhibit subsequent dispersal responses to NO. Finally, the addition of imidazole, which can inhibit the NO dioxygenase activity of flavohemoglobin, attenuated the prevention of dispersal after NO pretreatment and improved the dispersal response in older, starved biofilms. This study clarifies the underlying mechanisms of impaired dispersal induced by repeated NO treatments and offers a new perspective for improving the use of NO in biofilm control strategies.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/124082