Toll-like receptors recognize uropathogenic Escherichia coli and trigger inflammation in the urinary tract

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 [2–4]. 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 innate immunity. Thus, which receptors recognize uropathogenic pathogens, and what are the subsequent signalling cascades that concert antibacterial immunity? The recent discovery of the Toll-like receptor (TLR) family has identified a group of such receptors that appear to have important functions not only for pathogen recognition but also for innate immune activation [5]. In this article, we present the current view on TLRs in UTI. Based on these data, we propose a working hypothesis and raise new questions that deserve further study in this field.