Intramacrophage survival of uropathogenic Escherichia coli: Differences between diverse clinical isolates and between mouse and human macrophages

Handle URI:
http://hdl.handle.net/10754/561905
Title:
Intramacrophage survival of uropathogenic Escherichia coli: Differences between diverse clinical isolates and between mouse and human macrophages
Authors:
Bokil, Nilesh J.; Totsika, Makrina; Carey, Alison J.; Stacey, Katryn J.; Hancock, Viktoria; Saunders, Bernadette M.; Ravasi, Timothy ( 0000-0002-9950-465X ) ; Ulett, Glen C.; Schembri, Mark A.; Sweet, Matthew J.
Abstract:
Uropathogenic E. coli (UPEC) are the primary cause of urinary tract infections. Recent studies have demonstrated that UPEC can invade and replicate within epithelial cells, suggesting that this bacterial pathogen may occupy an intracellular niche within the host. Given that many intracellular pathogens target macrophages, we assessed the interactions between UPEC and macrophages. Colonization of the mouse bladder by UPEC strain CFT073 resulted in increased expression of myeloid-restricted genes, consistent with the recruitment of inflammatory macrophages to the site of infection. In in vitro assays, CFT073 was able to survive within primary mouse bone marrow-derived macrophages (BMM) up to 24h post-infection. Three additional well-characterized clinical UPEC isolates associated with distinct UTI symptomatologies displayed variable long-term survival within BMM. UPEC strains UTI89 and VR50, originally isolated from patients with cystitis and asymptomatic bacteriuria respectively, showed elevated bacterial loads in BMM at 24h post-infection as compared to CFT073 and the asymptomatic bacteriuria strain 83972. These differences did not correlate with differential effects on macrophage survival or initial uptake of bacteria. E. coli UTI89 localized to a Lamp1 + vesicular compartment within BMM. In contrast to survival within mouse BMM, intracellular bacterial loads of VR50 were low in both human monocyte-derived macrophages (HMDM) and in human T24 bladder epithelial cells. Collectively, these data suggest that some UPEC isolates may subvert macrophage anti-microbial pathways, and that host species differences may impact on intracellular UPEC survival. © 2011 Elsevier GmbH.
KAUST Department:
Applied Mathematics and Computational Science Program; Biological and Environmental Sciences and Engineering (BESE) Division; Red Sea Research Center (RSRC); Bioscience Program; Computational Bioscience Research Center (CBRC); Integrative Systems Biology Lab
Publisher:
Elsevier
Journal:
Immunobiology
Issue Date:
Nov-2011
DOI:
10.1016/j.imbio.2011.05.011
PubMed ID:
21802164
Type:
Article
ISSN:
01712985
Sponsors:
This work was supported by project grants from the National Health and Medical Research Council of Australia (APP1005315, 631531 and 569674). KJS, MAS and MJS are supported by ARC Future Fellowships, and MJS is supported by an honorary NHMRC Senior Research Fellowship. Confocal microscopy was performed at the Australian Cancer Research Foundation (ACRF)/Institute for Molecular Bioscience Dynamic Imaging Facility for Cancer Biology, which was established with the support of the ACRF. We thank Prof. Scott Hultgren for providing strain UTI89.
Appears in Collections:
Articles; Red Sea Research Center (RSRC); Bioscience Program; Applied Mathematics and Computational Science Program; Computational Bioscience Research Center (CBRC); Biological and Environmental Sciences and Engineering (BESE) Division

Full metadata record

DC FieldValue Language
dc.contributor.authorBokil, Nilesh J.en
dc.contributor.authorTotsika, Makrinaen
dc.contributor.authorCarey, Alison J.en
dc.contributor.authorStacey, Katryn J.en
dc.contributor.authorHancock, Viktoriaen
dc.contributor.authorSaunders, Bernadette M.en
dc.contributor.authorRavasi, Timothyen
dc.contributor.authorUlett, Glen C.en
dc.contributor.authorSchembri, Mark A.en
dc.contributor.authorSweet, Matthew J.en
dc.date.accessioned2015-08-03T09:33:46Zen
dc.date.available2015-08-03T09:33:46Zen
dc.date.issued2011-11en
dc.identifier.issn01712985en
dc.identifier.pmid21802164en
dc.identifier.doi10.1016/j.imbio.2011.05.011en
dc.identifier.urihttp://hdl.handle.net/10754/561905en
dc.description.abstractUropathogenic E. coli (UPEC) are the primary cause of urinary tract infections. Recent studies have demonstrated that UPEC can invade and replicate within epithelial cells, suggesting that this bacterial pathogen may occupy an intracellular niche within the host. Given that many intracellular pathogens target macrophages, we assessed the interactions between UPEC and macrophages. Colonization of the mouse bladder by UPEC strain CFT073 resulted in increased expression of myeloid-restricted genes, consistent with the recruitment of inflammatory macrophages to the site of infection. In in vitro assays, CFT073 was able to survive within primary mouse bone marrow-derived macrophages (BMM) up to 24h post-infection. Three additional well-characterized clinical UPEC isolates associated with distinct UTI symptomatologies displayed variable long-term survival within BMM. UPEC strains UTI89 and VR50, originally isolated from patients with cystitis and asymptomatic bacteriuria respectively, showed elevated bacterial loads in BMM at 24h post-infection as compared to CFT073 and the asymptomatic bacteriuria strain 83972. These differences did not correlate with differential effects on macrophage survival or initial uptake of bacteria. E. coli UTI89 localized to a Lamp1 + vesicular compartment within BMM. In contrast to survival within mouse BMM, intracellular bacterial loads of VR50 were low in both human monocyte-derived macrophages (HMDM) and in human T24 bladder epithelial cells. Collectively, these data suggest that some UPEC isolates may subvert macrophage anti-microbial pathways, and that host species differences may impact on intracellular UPEC survival. © 2011 Elsevier GmbH.en
dc.description.sponsorshipThis work was supported by project grants from the National Health and Medical Research Council of Australia (APP1005315, 631531 and 569674). KJS, MAS and MJS are supported by ARC Future Fellowships, and MJS is supported by an honorary NHMRC Senior Research Fellowship. Confocal microscopy was performed at the Australian Cancer Research Foundation (ACRF)/Institute for Molecular Bioscience Dynamic Imaging Facility for Cancer Biology, which was established with the support of the ACRF. We thank Prof. Scott Hultgren for providing strain UTI89.en
dc.publisherElsevieren
dc.subjectBacterial pathogenen
dc.subjectBladder infectionen
dc.subjectHost defenceen
dc.subjectMacrophageen
dc.subjectSpecies differencesen
dc.subjectToll-like receptoren
dc.subjectUPECen
dc.titleIntramacrophage survival of uropathogenic Escherichia coli: Differences between diverse clinical isolates and between mouse and human macrophagesen
dc.typeArticleen
dc.contributor.departmentApplied Mathematics and Computational Science Programen
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Divisionen
dc.contributor.departmentRed Sea Research Center (RSRC)en
dc.contributor.departmentBioscience Programen
dc.contributor.departmentComputational Bioscience Research Center (CBRC)en
dc.contributor.departmentIntegrative Systems Biology Laben
dc.identifier.journalImmunobiologyen
dc.contributor.institutionThe University of Queensland, Institute for Molecular Bioscience, Qld 4072, Australiaen
dc.contributor.institutionThe University of Queensland, School of Chemistry and Molecular Biosciences, Qld 4072, Australiaen
dc.contributor.institutionCentre for Medicine and Oral Health, Griffith University, Southport 4222, Australiaen
dc.contributor.institutionThe University of Queensland, Australian Infectious Diseases Research Centre, Qld 4072, Australiaen
dc.contributor.institutionDTU Food, Technical University of Denmark, Lyngby, Denmarken
dc.contributor.institutionMycobacterial Research Program, Centenary Institute, NSW 2042, Australiaen
kaust.authorRavasi, Timothyen

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