dc.contributor.author | Chamoun, Michelle N | |
dc.contributor.author | Sullivan, Matthew J | |
dc.contributor.author | Goh, Kelvin GK | |
dc.contributor.author | Acharya, Dhruba | |
dc.contributor.author | Ipe, Deepak S | |
dc.contributor.author | Katupitiya, Lahiru | |
dc.contributor.author | Gosling, Dean | |
dc.contributor.author | Peters, Kate M | |
dc.contributor.author | Sweet, Matthew J | |
dc.contributor.author | Sester, David P | |
dc.contributor.author | Schembri, Mark A | |
dc.contributor.author | Ulett, Glen C | |
dc.date.accessioned | 2020-09-17T03:36:26Z | |
dc.date.available | 2020-09-17T03:36:26Z | |
dc.date.issued | 2020 | |
dc.identifier.issn | 1530-6860 | |
dc.identifier.doi | 10.1096/fj.202000760R | |
dc.identifier.uri | http://hdl.handle.net/10072/397605 | |
dc.description.abstract | Urinary tract infections (UTI) frequently progress to chronicity in infected individuals but the mechanisms of pathogenesis underlying chronic UTI are not well understood. We examined the role of interleukin (IL)-17A in UTI because this cytokine promotes innate defense against uropathogenic Escherichia coli (UPEC). Analysis of UPEC persistence and pyelonephritis in mice deficient in IL-17A revealed that UPEC CFT073 caused infection at a rate higher than the multidrug resistant strain EC958. Il17a-/- mice exhibited pyelonephritis with kidney bacterial burdens higher than those of wild-type (WT) mice. Synthesis of IL-17A in the bladder reflected a combination of γδ-T and TH 17 cell responses. Analysis of circulating inflammatory mediators at 24h postinoculation identified predictors of progression to chronicity, including IL-6 and monocyte chemoattractant protein-1 (MCP-1). Histological analysis identified infiltrating populations of neutrophils, NK cells, and γδ T cells in the bladder, whereas neutrophils predominated in the kidney. Analysis of the contribution of flagella to chronicity using hyper-flagellated and fliC-deficient UPEC in WT and Il17a-/- mice revealed that, in a host that is deficient for the production of IL-17A, flagella contribute to bacterial persistence. These findings show a role for IL-17A in defense against chronic UTI and a contribution of flagella to the pathogenesis of infection. | |
dc.description.peerreviewed | Yes | |
dc.language | English | |
dc.language.iso | eng | |
dc.publisher.uri | https://faseb.onlinelibrary.wiley.com/doi/10.1096/fj.202000760R | |
dc.relation.ispartofjournal | FASEB Journal | |
dc.subject.fieldofresearch | Biochemistry and cell biology | |
dc.subject.fieldofresearch | Zoology | |
dc.subject.fieldofresearch | Medical physiology | |
dc.subject.fieldofresearchcode | 3101 | |
dc.subject.fieldofresearchcode | 3109 | |
dc.subject.fieldofresearchcode | 3208 | |
dc.subject.keywords | Escherichia coli | |
dc.subject.keywords | Gram-negative pathogens | |
dc.subject.keywords | bacterial pathogenesis | |
dc.subject.keywords | innate immunity | |
dc.subject.keywords | urinary tract infection | |
dc.title | Restriction of chronic Escherichia coli urinary tract infection depends upon T cell-derived interleukin-17, a deficiency of which predisposes to flagella-driven bacterial persistence | |
dc.type | Journal article | |
dc.type.description | C1 - Articles | |
dcterms.bibliographicCitation | Chamoun, MN; Sullivan, MJ; Goh, KGK; Acharya, D; Ipe, DS; Katupitiya, L; Gosling, D; Peters, KM; Sweet, MJ; Sester, DP; Schembri, MA; Ulett, GC, Restriction of chronic Escherichia coli urinary tract infection depends upon T cell-derived interleukin-17, a deficiency of which predisposes to flagella-driven bacterial persistence., FASEB Journal, 2020 | |
dcterms.dateAccepted | 2020-08-18 | |
dc.date.updated | 2020-09-17T02:38:23Z | |
gro.description.notepublic | This publication has been entered into Griffith Research Online as an Advanced Online Version. | |
gro.hasfulltext | No Full Text | |
gro.griffith.author | Ulett, Glen C. | |
gro.griffith.author | Acharya, Dhruba | |