Show simple item record

dc.contributor.authorBokil, Nilesh J
dc.contributor.authorTotsika, Makrina
dc.contributor.authorCarey, Alison J
dc.contributor.authorStacey, Katryn J
dc.contributor.authorHancock, Viktoria
dc.contributor.authorSaunders, Bernadette M
dc.contributor.authorRavasi, Timothy
dc.contributor.authorUlett, Glen C
dc.contributor.authorSchembri, Mark A
dc.contributor.authorSweet, Matthew J
dc.date.accessioned2017-05-03T15:29:33Z
dc.date.available2017-05-03T15:29:33Z
dc.date.issued2011
dc.date.modified2012-02-14T05:34:18Z
dc.identifier.issn0171-2985
dc.identifier.doi10.1016/j.imbio.2011.05.011
dc.identifier.urihttp://hdl.handle.net/10072/42595
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.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherElsevier
dc.publisher.placeGermany
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom1164
dc.relation.ispartofpageto1171
dc.relation.ispartofissue11
dc.relation.ispartofjournalImmunobiology
dc.relation.ispartofvolume216
dc.rights.retentionY
dc.subject.fieldofresearchBiological sciences
dc.subject.fieldofresearchAgricultural, veterinary and food sciences
dc.subject.fieldofresearchBiomedical and clinical sciences
dc.subject.fieldofresearchMedical bacteriology
dc.subject.fieldofresearchcode31
dc.subject.fieldofresearchcode30
dc.subject.fieldofresearchcode32
dc.subject.fieldofresearchcode320701
dc.titleIntramacrophage survival of uropathogenic Escherichia coli: Differences between diverse clinical isolates and between mouse and human macrophages
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.date.issued2011
gro.hasfulltextNo Full Text
gro.griffith.authorUlett, Glen C.


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following Collection(s)

  • Journal articles
    Contains articles published by Griffith authors in scholarly journals.

Show simple item record