Role of IL-17A in the development of chronic UPEC urinary tract infeciton — ASN Events
  1. Schedule
  2. Poster Session One & Burnet Oration Cocktail Function
  3. Role of IL-17A in the development of chronic UPEC urinary tract infeciton

Role of IL-17A in the development of chronic UPEC urinary tract infeciton (#182)

Michelle N Chamoun 1 , Deepak S Ipe 1 , Matthew J Sullivan 1 , Mark A Schembri 2 3 , Glen C Ulett 1 4
  1. School of Medical Science, Menzies health institute Queensland, Griffith Univerisity, Southport, Queensland, Australia
  2. School of Chemistry and Molecular Biosciences, University of Queensland, Brisbane, Queensland, Australia
  3. Australian Infectious Diseases Research Centre, University of Queensland, Brisbane, Queensland, Australia
  4. School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA

Chronic recurrent urinary tract infection (rUTI) occurs in up to 50% of women following an initial acute UTI episode1. However, the nature of the immune response that develops during chronic rUTI is incompletely characterized. Interleukin-17A (IL-17A) has been identified as an important cytokine in the control of acute UTI during the innate phase of infection2; however, the role of IL-17A in chronic rUTI has not been investigated.


We investigated this cytokine in the control of chronic UTI in mice, using a superinfection model with uropathogenic Escherichia coli (UPEC). Female Balb/c wild type (WT) or IL-17A-/- mice were superinfected with two doses of either UPEC strain EC958 or CFT073, 24h apart. Infection was monitored at multiple time points over 28 days by enumerating bacterial loads in urine as colony forming units (CFU)/ml, with the number of bacteria in the bladder and kidneys assessed at 28 days. Histology and enzyme-linked immunosorbance assay (ELISA) analysis were used to examine tissue infiltrates and local IL-17A levels.


CFT073-superinfected and EC958-superinfected IL-17-/- mice had significantly higher CFU/ml compared to WT mice at day 1 and day 21 post-infection, respectively. Both CFT073 and EC958-superinfected mice had significantly higher bladder and kidney counts at day 28 compared to WT mice. Analysis of IL-17A in the bladders of chronically-infected WT mice revealed elevated IL-17A levels compared to mice that spontaneously resolved. Histopathology analysis showed increased inflammatory cell infiltration in the kidneys of EC958-infected IL-17A-/- mice compared EC958-infected WT mice. CFT073-infected IL-17-/- mice had more inflammatory cell infiltrates compared to EC958-infected IL-17-/- mice.


Together, these data show that IL-17A is important in preventing chronic UTI by two different but well-characterised UPEC strains. Elevated IL-17A levels in chronically-infected WT mice, and increased numbers of mixed inflammatory cell infiltrates in IL-17A-/- mice, suggest an important role for IL-17A that warrants further study.

  1. Foxman, B., Urinary tract infection syndromes: occurrence, recurrence, bacteriology, risk factors, and disease burden. Infectious Disease Clinics of North America, 2014. 28(1): p. 1-13.
  2. Sivick, K.E., et al., The innate immune response to uropathogenic Escherichia coli involves IL-17A in a murine model of urinary tract infection. Journal of Immunology, 2010. 184(4): p. 2065-75.
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