Urinary tract infections (UTI) are the second most common infectious disease, incurring significant medical costs and resulting in widespread morbidity and mortality worldwide. Most UTI are caused by Escherichia coli colonization of the urethra and ascension into the bladder causing cystitis. Pyelonephritis can develop as a consequence of bacteria ascending the ureters leading to kidney scarring and kidney failure. Efficient peristalsis is therefore vital in maintaining renal health. E.coli colonization can impair ureteric contractility and cause dilation which in turn potentiates infection due to urinary stasis and/or vesicoureteric reflux but little is known about the mechanisms of impaired ureteric function. In this presentation I will show how exposure of rat and human ureters to uropathogenic E.coli (UPEC) causes changes in phasic contractions and Ca²⁺ transients evoked by electrical field stimulation and suggest underlying mechanisms. The physiological effects of blocking type-1 fimbrial binding by pre-incubation of UPEC with mannose will be presented and strain-specific differences will be discussed in detail in light of current understanding of how host and pathogen interact in the urinary tract. Recent studies in animal bladder have given insight into the invasive potential of sub-types of UPEC, which increases their capacity to cause recurrent disease. These findings will be reviewed and preliminary data from our group investigating these mechanisms in ureter which show that UPEC have the capacity to invade and replicate within urothelial cells, will be presented. These multidisciplinary approaches allow us to further understand ureter physiology and pathophysiology which can be translated into clinical benefit for patients affected by recurrent and persistent UTI.