The co-transcriptome of uropathogenic Escherichia coli-infected mouse macrophages reveals new insights into host-pathogen interactions

Handle URI:
http://hdl.handle.net/10754/550523
Title:
The co-transcriptome of uropathogenic Escherichia coli-infected mouse macrophages reveals new insights into host-pathogen interactions
Authors:
Mavromatis, Charalampos Harris ( 0000-0002-7327-231X ) ; Bokil, Nilesh J.; Totsika, Makrina; Kakkanat, Asha; Schaale, Kolja; Cannistraci, Carlo V.; Ryu, Tae Woo; Beatson, Scott A.; Ulett, Glen C.; Schembri, Mark A.; Sweet, Matthew J.; Ravasi, Timothy ( 0000-0002-9950-465X )
Abstract:
Urinary tract infections (UTI) are among the most common infections in humans. Uropathogenic Escherichia coli (UPEC) can invade and replicate within bladder epithelial cells, and some UPEC strains can also survive within macrophages. To understand the UPEC transcriptional programme associated with intramacrophage survival, we performed host–pathogen co-transcriptome analyses using RNA sequencing. Mouse bone marrow-derived macrophages (BMMs) were challenged over a 24 h time course with two UPEC reference strains that possess contrasting intramacrophage phenotypes: UTI89, which survives in BMMs, and 83972, which is killed by BMMs. Neither of these strains caused significant BMM cell death at the low multiplicity of infection that was used in this study. We developed an effective computational framework that simultaneously separated, annotated and quantified the mammalian and bacterial transcriptomes. Bone marrow-derived macrophages responded to the two UPEC strains with a broadly similar gene expression programme. In contrast, the transcriptional responses of the UPEC strains diverged markedly from each other. We identified UTI89 genes up-regulated at 24 h post-infection, and hypothesized that some may contribute to intramacrophage survival. Indeed, we showed that deletion of one such gene (pspA) significantly reduced UTI89 survival within BMMs. Our study provides a technological framework for simultaneously capturing global changes at the transcriptional level in co-cultures, and has generated new insights into the mechanisms that UPEC use to persist within the intramacrophage environment.
KAUST Department:
Biological and Environmental Sciences and Engineering (BESE) Division; Computer, Electrical and Mathematical Sciences and Engineering (CEMSE) Division
Citation:
The co-transcriptome of uropathogenic Escherichia coli-infected mouse macrophages reveals new insights into host-pathogen interactions, 2015, 17 (5):730 Cellular Microbiology
Publisher:
Wiley-Blackwell
Journal:
Cellular Microbiology
Issue Date:
24-Jan-2015
DOI:
10.1111/cmi.12397
Type:
Article
ISSN:
14625814
Additional Links:
http://doi.wiley.com/10.1111/cmi.12397
Appears in Collections:
Articles; Biological and Environmental Sciences and Engineering (BESE) Division; Computer, Electrical and Mathematical Sciences and Engineering (CEMSE) Division

Full metadata record

DC FieldValue Language
dc.contributor.authorMavromatis, Charalampos Harrisen
dc.contributor.authorBokil, Nilesh J.en
dc.contributor.authorTotsika, Makrinaen
dc.contributor.authorKakkanat, Ashaen
dc.contributor.authorSchaale, Koljaen
dc.contributor.authorCannistraci, Carlo V.en
dc.contributor.authorRyu, Tae Wooen
dc.contributor.authorBeatson, Scott A.en
dc.contributor.authorUlett, Glen C.en
dc.contributor.authorSchembri, Mark A.en
dc.contributor.authorSweet, Matthew J.en
dc.contributor.authorRavasi, Timothyen
dc.date.accessioned2015-04-23T14:17:35Zen
dc.date.available2015-04-23T14:17:35Zen
dc.date.issued2015-01-24en
dc.identifier.citationThe co-transcriptome of uropathogenic Escherichia coli-infected mouse macrophages reveals new insights into host-pathogen interactions, 2015, 17 (5):730 Cellular Microbiologyen
dc.identifier.issn14625814en
dc.identifier.doi10.1111/cmi.12397en
dc.identifier.urihttp://hdl.handle.net/10754/550523en
dc.description.abstractUrinary tract infections (UTI) are among the most common infections in humans. Uropathogenic Escherichia coli (UPEC) can invade and replicate within bladder epithelial cells, and some UPEC strains can also survive within macrophages. To understand the UPEC transcriptional programme associated with intramacrophage survival, we performed host–pathogen co-transcriptome analyses using RNA sequencing. Mouse bone marrow-derived macrophages (BMMs) were challenged over a 24 h time course with two UPEC reference strains that possess contrasting intramacrophage phenotypes: UTI89, which survives in BMMs, and 83972, which is killed by BMMs. Neither of these strains caused significant BMM cell death at the low multiplicity of infection that was used in this study. We developed an effective computational framework that simultaneously separated, annotated and quantified the mammalian and bacterial transcriptomes. Bone marrow-derived macrophages responded to the two UPEC strains with a broadly similar gene expression programme. In contrast, the transcriptional responses of the UPEC strains diverged markedly from each other. We identified UTI89 genes up-regulated at 24 h post-infection, and hypothesized that some may contribute to intramacrophage survival. Indeed, we showed that deletion of one such gene (pspA) significantly reduced UTI89 survival within BMMs. Our study provides a technological framework for simultaneously capturing global changes at the transcriptional level in co-cultures, and has generated new insights into the mechanisms that UPEC use to persist within the intramacrophage environment.en
dc.publisherWiley-Blackwellen
dc.relation.urlhttp://doi.wiley.com/10.1111/cmi.12397en
dc.rightsThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.en
dc.titleThe co-transcriptome of uropathogenic Escherichia coli-infected mouse macrophages reveals new insights into host-pathogen interactionsen
dc.typeArticleen
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Divisionen
dc.contributor.departmentComputer, Electrical and Mathematical Sciences and Engineering (CEMSE) Divisionen
dc.identifier.journalCellular Microbiologyen
dc.eprint.versionPublisher's Version/PDFen
dc.contributor.institutionInstitute for Molecular Bioscience; The University of Queensland; St Lucia Queensland Australiaen
dc.contributor.institutionAustralian Infectious Diseases Research Centre; The University of Queensland; St Lucia Queensland Australiaen
dc.contributor.institutionAustralian Infectious Diseases Research Centre; The University of Queensland; St Lucia Queensland Australiaen
dc.contributor.institutionInstitute for Molecular Bioscience; The University of Queensland; St Lucia Queensland Australiaen
dc.contributor.institutionAustralian Infectious Diseases Research Centre; The University of Queensland; St Lucia Queensland Australiaen
dc.contributor.institutionGriffith Health Institute and School of Medical Science, Griffith Health Centre, Gold Coast Campus; Griffith University; Southport Queensland 4222 Australiaen
dc.contributor.institutionAustralian Infectious Diseases Research Centre; The University of Queensland; St Lucia Queensland Australiaen
dc.contributor.institutionInstitute for Molecular Bioscience; The University of Queensland; St Lucia Queensland Australiaen
dc.contributor.institutionDivision of Medical Genetics, Department of Medicine, University of California, San Diego, La Jolla, CA, USAen
dc.contributor.institutionSchool of Chemistry and Molecular Biosciences, The University of Queensland, St Lucia, Queensland, Australiaen
dc.contributor.institutionInstitute of Health and Biomedical Innovation (IHBI), School of Biomedical Sciences, Queensland University of Technology (QUT), Kelvin Grove, Queensland, Australiaen
dc.contributor.institutionBiomedical Cybernetics Group, Biotechnology Center (BIOTEC), Technische Universität Dresden, Dresden, Germanyen
kaust.authorMavromatis, Charalampos Harrisen
kaust.authorCannistraci, Carloen
kaust.authorRyu, Tae Wooen
kaust.authorRavasi, Timothyen
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