Urinary tract infections (UTIs) are among the most common bacterial infections, predominantly caused by Uropathogenic Escherichia coli (UPEC). Current antibiotic treatments are failing and have driven the rise of multi-drug-resistant bacteria. Asymptomatic bacteriuria is the colonisation of bacteria in the bladder without clinical symptoms and has been suggested to protect against symptomatic UTIs through bacterial interference. This project aimed to establish the behaviour of an isolate from an asymptomatic catheter-associated UTI during in vitro single-strain UTI models and then determine its effect during dual-strain models. This study used an asymptomatic isolate, a non-pathogenic E. coli strain, and a symptomatic UPEC strain. Single-strain infections of each strain were conducted to quantify the percentage of invasion into immortalised human bladder epithelial cells. A dual-strain model combining the asymptomatic isolate with the symptomatic strain was also conducted, and the percentage invasion was compared to the single-strain models. Invasion was quantified by the number of invaded bladder cells observed from acquired Z-stacks on a confocal microscope. The single-strain infections revealed that the asymptomatic isolate followed a similar invasion cycle previously observed in the symptomatic strain. This was observed with the formation of intracellular bacterial communities within bladder cells and adopting a filamentous morphology during late-stage invasion. During dual-strain infections, however, it was found that the asymptomatic isolate did not affect the invasion of the symptomatic strain. The co-existence of both strains in the same bladder cell was observed, and both formed filaments in the same infection. This suggests that asymptomatic isolates may share similar survival strategies with symptomatic UPEC strains, raising questions concerning the correlation between bladder cell invasion and virulence. Additionally, the asymptomatic strain in this study could not be recommended as a potential candidate for bacterial interference due to its inability to significantly hinder the invasion of the symptomatic strain.