NDT Advance Access originally published online on June 7, 2005
Nephrology Dialysis Transplantation 2005 20(8):1529-1532; doi:10.1093/ndt/gfh922
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Editorial Comment
Toll-like receptors recognize uropathogenic Escherichia coli and trigger inflammation in the urinary tract
Nephrological Center, Medical Policlinic, Ludwig-Maximilians-University, Munich, Germany
Correspondence and offprint requests to: Dr H.-J. Anders, Medizinische Poliklinik der LMU, Pettenkoferstr. 8a, D-80336 Munich, Germany. Email: hjanders@med.uni-muenchen.de
Keywords: chemokines; immunity; infection; leukocytes
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| Introduction |
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Urinary tract infection (UTI) is one of the most common types of infection. In the USA, >US$1.6 billion per year are spent in the management of UTI [1]. Amongst the pathogens that can cause UTI, uropathogenic Escherichia coli (UPEC) has been found to be the causative organism in
80% of cases. A number of pathogen-related virulence factors have been identified that relate mostly to pathogen adhesion to the epithelial lining of the urinary tract [24]. In addition, patient-related factors determine the prevalence and severity of UTI. Diabetes, immunosuppression, reflux and obstruction due to structural abnormalities of the urinary tract or pregnancy are known to predispose to UTI. These conditions affect either physiological urine flow or cellular immunity against uropathogenic agents. However, the patient-related risk for UTI may also be determined by pathogen recognition and pathogen-induced signalling for host defence. Host defence in UTI is based on | Toll-like receptors are innate pathogen recognition receptors |
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| TLR4 and TLR11 signal for renal neutrophil recruitment in mice with UTI |
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| Do intrinsic renal cells signal through TLRs during UPEC infection? |
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| Are data from mouse models relevant for human UTI? |
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| Future directions |
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