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      Genetic Risk for Recurrent Urinary Tract Infections in Humans: A Systematic Review

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          Abstract

          Urinary tract infections (UTIs) are a frequent cause of morbidity in children and adults and affect up to 10% of children; its recurrence rate is estimated at 30–40%. UTI may occur in up to 50% of all women in their lifetimes and frequently require medication. Recent advances have suggested that a deregulation of candidate genes in humans may predispose patients to recurrent UTI. The identification of a genetic component of UTI recurrences will make it possible to diagnose at-risk adults and to predict genetic recurrences in their offspring. Six out of 14 genes investigated in humans may be associated with susceptibility to recurrent UTI in humans. In particular, the HSPA1B, CXCR1 & 2, TLR2, TLR4, TGF- β1 genes seem to be associated with an alteration of the host response to UTIs at various levels.

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          Risk factors for recurrent urinary tract infection in young women.

          Timothy Roberts, James A. Stapleton, D Scholes … (2000)
          To define host factors associated with an increased risk of recurrent urinary tract infection (RUTI), a case-control study was conducted in 2 populations: university women and health maintenance organization enrollees. Case patients were 229 women 18-30 years old with RUTIs; control subjects were 253 randomly selected women with no RUTI history. In a multivariate model, independent risk factors for RUTI included recent 1-month intercourse frequency (odds ratio [OR], 5.8; 95% confidence interval [CI], 3.1-10.6 for 4-8 episodes), 12-month spermicide use (OR, 1.8; 95% CI, 1.1-2.9), and new sex partner during the past year (OR, 1.9; 95% CI, 1.2-3.2). Two newly identified risk factors were age at first urinary tract infection (UTI)
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            Toll-Like Receptor Polymorphisms and Susceptibility to Urinary Tract Infections in Adult Women

            Thomas R. Hawn, Delia Scholes, Shuying Li … (2009)
            Background Although behavioral risk factors are strongly associated with urinary tract infection (UTI) risk, the role of genetics in acquiring this disease is poorly understood. Methodology/Principal Findings To test the hypothesis that polymorphisms in Toll-like receptor (TLR) pathway genes are associated with susceptibility to UTIs, we conducted a population-based case-control study of women ages 18–49 years. We examined DNA variants in 9 TLR pathway genes in 431 recurrent cystitis (rUTI) cases, 400 pyelonephritis cases, and 430 controls with no history of UTIs. In the Caucasian subgroup of 987 women, polymorphism TLR4_A896G was associated with protection from rUTI, but not pyelonephritis, with an odds ratio (OR) of 0.54 and a 95% confidence interval (CI) of 0.31 to 0.96. Polymorphism TLR5_C1174T, which encodes a variant that abrogates flagellin-induced signaling, was associated with an increased risk of rUTI (OR(95%CI): 1.81 (1.00–3.08)), but not pyelonephritis. Polymorphism TLR1_G1805T was associated with protection from pyelonephritis (OR(95%CI): 0.53 (0.29–0.96)). Conclusions These results provide the first evidence of associations of TLR5 and TLR1 variants with altered risks of acquiring rUTI and pyelonephritis, respectively. Although these data suggest that TLR polymorphisms are associated with adult susceptibility to UTIs, the statistical significance was modest and will require further study including validation with independent cohorts.
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              Interleukin 8 Receptor Deficiency Confers Susceptibility to Acute Experimental Pyelonephritis and May Have a Human Counterpart

              Björn Frendéus, Gabriela Godaly, Long Hang … (2000)
              Neutrophils migrate to infected mucosal sites that they protect against invading pathogens. Their interaction with the epithelial barrier is controlled by CXC chemokines and by their receptors. This study examined the change in susceptibility to urinary tract infection (UTI) after deletion of the murine interleukin 8 receptor homologue (mIL-8Rh). Experimental UTIs in control mice stimulated an epithelial chemokine response and increased chemokine receptor expression. Neutrophils migrated through the tissues to the epithelial barrier that they crossed into the lumen, and the mice developed pyuria. In mIL-8Rh knockout (KO) mice, the chemokine response was intact, but the epithelial cells failed to express IL-8R, and neutrophils accumulated in the tissues. The KO mice were unable to clear bacteria from kidneys and bladders and developed bacteremia and symptoms of systemic disease, but control mice were fully resistant to infection. The experimental UTI model demonstrated that IL-8R–dependent mechanisms control the urinary tract defense, and that neutrophils are essential host effector cells. Patients prone to acute pyelonephritis also showed low CXC chemokine receptor 1 expression compared with age-matched controls, suggesting that chemokine receptor expression may also influence the susceptibility to UTIs in humans. The results provide a first molecular clue to disease susceptibility of patients prone to acute pyelonephritis.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Biomed Biotechnol
                Journal ID (publisher-id): JBB
                Title: Journal of Biomedicine and Biotechnology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 1110-7243
                ISSN (Electronic): 1110-7251
                Publication date (Print): 2010
                Publication date (Electronic): 30 March 2010
                Volume: 2010
                Electronic Location Identifier: 321082
                Affiliations
                1Department of Mother-Child and Biology-Genetics, Section of Pediatrics, University of Verona, Piazzale L. Scuro, 10, 37134 Verona, Italy
                2Department of Mother and Child and Biology-Genetics, Section of Biology and Genetics, University of Verona, Verona 37134, Italy
                3Division of Neonatology, Catholic University of the Sacred Heart, Rome 00168, Italy
                4Department of Pathology and Laboratory Medicine, Immunohematology and Transfusion Center, University Hospital of Parma, Parma 43121, Italy
                5Neonatal Intensive Care Unit, University of Cagliari, Cagliari 09124, Italy
                Author notes

                Academic Editor: Wenjiang J. Fu

                Article
                DOI: 10.1155/2010/321082
                PMC ID: 2847765
                PubMed ID: 20379347
                SO-VID: 59ea3838-d53a-4c24-902b-a8698bd6d67b
                Copyright © Copyright © 2010 M. Zaffanello et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 31 July 2009
                Date accepted : 25 February 2010
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Molecular medicine
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                ScienceOpen disciplines: Molecular medicine

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