Temperate phages enhance pathogen fitness in chronic lung infection
The Liverpool Epidemic Strain (LES) is a polylysogenic, transmissible strain of Pseudomonas aeruginosa , capable of superinfecting existing P. aeruginosa respiratory infections in individuals with cystic fibrosis (CF). The LES phages are highly active in the CF lung and may have a role in the compet...
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description | The Liverpool Epidemic Strain (LES) is a polylysogenic, transmissible strain of
Pseudomonas aeruginosa
, capable of superinfecting existing
P. aeruginosa
respiratory infections in individuals with cystic fibrosis (CF). The LES phages are highly active in the CF lung and may have a role in the competitiveness of the LES
in vivo
. In this study, we tested this by competing isogenic PAO1 strains that differed only by the presence or absence of LES prophages in a rat model of chronic lung infection. Lysogens invaded phage-susceptible populations, both in head-to-head competition and when invading from rare, in the spatially structured, heterogeneous lung environment. Appreciable densities of free phages in lung tissue confirmed active phage lysis
in vivo
. Moreover, we observed lysogenic conversion of the phage-susceptible competitor. These results suggest that temperate phages may have an important role in the competitiveness of the LES in chronic lung infection by acting as anti-competitor weapons. |
doi_str_mv | 10.1038/ismej.2016.51 |
format | Article |
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Pseudomonas aeruginosa
, capable of superinfecting existing
P. aeruginosa
respiratory infections in individuals with cystic fibrosis (CF). The LES phages are highly active in the CF lung and may have a role in the competitiveness of the LES
in vivo
. In this study, we tested this by competing isogenic PAO1 strains that differed only by the presence or absence of LES prophages in a rat model of chronic lung infection. Lysogens invaded phage-susceptible populations, both in head-to-head competition and when invading from rare, in the spatially structured, heterogeneous lung environment. Appreciable densities of free phages in lung tissue confirmed active phage lysis
in vivo
. Moreover, we observed lysogenic conversion of the phage-susceptible competitor. These results suggest that temperate phages may have an important role in the competitiveness of the LES in chronic lung infection by acting as anti-competitor weapons.</description><identifier>ISSN: 1751-7362</identifier><identifier>EISSN: 1751-7370</identifier><identifier>DOI: 10.1038/ismej.2016.51</identifier><identifier>PMID: 27070941</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>45/77 ; 631/158/855 ; 692/420 ; Animals ; Bacteriophages - physiology ; Biomedical and Life Sciences ; Chronic Disease ; Ecology ; Evolutionary Biology ; Humans ; Life Sciences ; Lung - microbiology ; Lung - virology ; Lysogeny ; Microbial Ecology ; Microbial Genetics and Genomics ; Microbiology ; Pseudomonas aeruginosa ; Pseudomonas aeruginosa - physiology ; Pseudomonas Infections - microbiology ; Rats ; Respiratory Tract Infections - microbiology ; Short Communication</subject><ispartof>The ISME Journal, 2016-10, Vol.10 (10), p.2553-2555</ispartof><rights>The Author(s) 2016</rights><rights>Copyright Nature Publishing Group Oct 2016</rights><rights>Copyright © 2016 International Society for Microbial Ecology 2016 International Society for Microbial Ecology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c553t-efcaf369941c54f261c4d85c6e30400abe031a15a1dd57a2bdf20f297a62f6423</citedby><cites>FETCH-LOGICAL-c553t-efcaf369941c54f261c4d85c6e30400abe031a15a1dd57a2bdf20f297a62f6423</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4950967/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4950967/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,729,782,786,887,27931,27932,53798,53800</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27070941$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Davies, Emily V</creatorcontrib><creatorcontrib>James, Chloe E</creatorcontrib><creatorcontrib>Kukavica-Ibrulj, Irena</creatorcontrib><creatorcontrib>Levesque, Roger C</creatorcontrib><creatorcontrib>Brockhurst, Michael A</creatorcontrib><creatorcontrib>Winstanley, Craig</creatorcontrib><title>Temperate phages enhance pathogen fitness in chronic lung infection</title><title>The ISME Journal</title><addtitle>ISME J</addtitle><addtitle>ISME J</addtitle><description>The Liverpool Epidemic Strain (LES) is a polylysogenic, transmissible strain of
Pseudomonas aeruginosa
, capable of superinfecting existing
P. aeruginosa
respiratory infections in individuals with cystic fibrosis (CF). The LES phages are highly active in the CF lung and may have a role in the competitiveness of the LES
in vivo
. In this study, we tested this by competing isogenic PAO1 strains that differed only by the presence or absence of LES prophages in a rat model of chronic lung infection. Lysogens invaded phage-susceptible populations, both in head-to-head competition and when invading from rare, in the spatially structured, heterogeneous lung environment. Appreciable densities of free phages in lung tissue confirmed active phage lysis
in vivo
. Moreover, we observed lysogenic conversion of the phage-susceptible competitor. These results suggest that temperate phages may have an important role in the competitiveness of the LES in chronic lung infection by acting as anti-competitor weapons.</description><subject>45/77</subject><subject>631/158/855</subject><subject>692/420</subject><subject>Animals</subject><subject>Bacteriophages - physiology</subject><subject>Biomedical and Life Sciences</subject><subject>Chronic Disease</subject><subject>Ecology</subject><subject>Evolutionary Biology</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Lung - microbiology</subject><subject>Lung - virology</subject><subject>Lysogeny</subject><subject>Microbial Ecology</subject><subject>Microbial Genetics and Genomics</subject><subject>Microbiology</subject><subject>Pseudomonas aeruginosa</subject><subject>Pseudomonas aeruginosa - physiology</subject><subject>Pseudomonas Infections - microbiology</subject><subject>Rats</subject><subject>Respiratory Tract Infections - microbiology</subject><subject>Short Communication</subject><issn>1751-7362</issn><issn>1751-7370</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkU1r3DAQhkVoSdIkx16LoZdevNHIlrS-BMrSpoVALulZaOWRrcWWNpIdyL-vNpssSekhp5lhHt75eAn5DHQBtFpeujTiZsEoiAWHI3IKkkMpK0k_HHLBTsinlDaUcimEPCYnTFJJmxpOyeoOxy1GPWGx7XWHqUDfa29yqac-dOgL6yaPKRXOF6aPwTtTDLPvcm3RTC74c_LR6iHhxXM8I39-_rhb_Spvbq9_r77flIbzairRGm0r0eS5hteWCTB1u-RGYEVrSvUaaQUauIa25VKzdWsZtayRWjAraladkau97nZej9ga9FPUg9pGN-r4qIJ26m3Hu1514UHVDaeNkFng27NADPczpkmNLhkcBu0xzEnBkskGGMh3oQyAU75b6-s_6CbM0edP7CiomagrnqlyT5kYUopoD3sDVTsn1ZOTauek4pD5L6-PPdAv1mVgsQdSbvkO46ux_1X8CyDbqd0</recordid><startdate>20161001</startdate><enddate>20161001</enddate><creator>Davies, Emily V</creator><creator>James, Chloe E</creator><creator>Kukavica-Ibrulj, Irena</creator><creator>Levesque, Roger C</creator><creator>Brockhurst, Michael A</creator><creator>Winstanley, Craig</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7SN</scope><scope>7ST</scope><scope>7T7</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>SOI</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20161001</creationdate><title>Temperate phages enhance pathogen fitness in chronic lung infection</title><author>Davies, Emily V ; James, Chloe E ; Kukavica-Ibrulj, Irena ; Levesque, Roger C ; Brockhurst, Michael A ; Winstanley, Craig</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c553t-efcaf369941c54f261c4d85c6e30400abe031a15a1dd57a2bdf20f297a62f6423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>45/77</topic><topic>631/158/855</topic><topic>692/420</topic><topic>Animals</topic><topic>Bacteriophages - physiology</topic><topic>Biomedical and Life Sciences</topic><topic>Chronic Disease</topic><topic>Ecology</topic><topic>Evolutionary Biology</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>Lung - microbiology</topic><topic>Lung - virology</topic><topic>Lysogeny</topic><topic>Microbial Ecology</topic><topic>Microbial Genetics and Genomics</topic><topic>Microbiology</topic><topic>Pseudomonas aeruginosa</topic><topic>Pseudomonas aeruginosa - physiology</topic><topic>Pseudomonas Infections - microbiology</topic><topic>Rats</topic><topic>Respiratory Tract Infections - microbiology</topic><topic>Short Communication</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Davies, Emily V</creatorcontrib><creatorcontrib>James, Chloe E</creatorcontrib><creatorcontrib>Kukavica-Ibrulj, Irena</creatorcontrib><creatorcontrib>Levesque, Roger C</creatorcontrib><creatorcontrib>Brockhurst, Michael A</creatorcontrib><creatorcontrib>Winstanley, Craig</creatorcontrib><collection>Springer Nature OA/Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Ecology Abstracts</collection><collection>Environment Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Environmental Science Collection</collection><collection>Environment Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The ISME Journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Davies, Emily V</au><au>James, Chloe E</au><au>Kukavica-Ibrulj, Irena</au><au>Levesque, Roger C</au><au>Brockhurst, Michael A</au><au>Winstanley, Craig</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Temperate phages enhance pathogen fitness in chronic lung infection</atitle><jtitle>The ISME Journal</jtitle><stitle>ISME J</stitle><addtitle>ISME J</addtitle><date>2016-10-01</date><risdate>2016</risdate><volume>10</volume><issue>10</issue><spage>2553</spage><epage>2555</epage><pages>2553-2555</pages><issn>1751-7362</issn><eissn>1751-7370</eissn><abstract>The Liverpool Epidemic Strain (LES) is a polylysogenic, transmissible strain of
Pseudomonas aeruginosa
, capable of superinfecting existing
P. aeruginosa
respiratory infections in individuals with cystic fibrosis (CF). The LES phages are highly active in the CF lung and may have a role in the competitiveness of the LES
in vivo
. In this study, we tested this by competing isogenic PAO1 strains that differed only by the presence or absence of LES prophages in a rat model of chronic lung infection. Lysogens invaded phage-susceptible populations, both in head-to-head competition and when invading from rare, in the spatially structured, heterogeneous lung environment. Appreciable densities of free phages in lung tissue confirmed active phage lysis
in vivo
. Moreover, we observed lysogenic conversion of the phage-susceptible competitor. These results suggest that temperate phages may have an important role in the competitiveness of the LES in chronic lung infection by acting as anti-competitor weapons.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>27070941</pmid><doi>10.1038/ismej.2016.51</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 45/77 631/158/855 692/420 Animals Bacteriophages - physiology Biomedical and Life Sciences Chronic Disease Ecology Evolutionary Biology Humans Life Sciences Lung - microbiology Lung - virology Lysogeny Microbial Ecology Microbial Genetics and Genomics Microbiology Pseudomonas aeruginosa Pseudomonas aeruginosa - physiology Pseudomonas Infections - microbiology Rats Respiratory Tract Infections - microbiology Short Communication |
title | Temperate phages enhance pathogen fitness in chronic lung infection |
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