| Urinary tract infections are the most common urologic disease in the United States and one of the most common bacterial infections of any organ system and uropathogenic E. coli are the most common pathogens associated with urinary tract and catheter infections. Urinary tract infections are difficult to treat because the bacteria grow in the form of a biofilm in the urinary tract or on catheter surfaces. The role of colanic acid in biofilm formation of uropathogenic E. coli was evaluated to determine its role in catheter-associated urinary tract infections. During early stages of biofilm formation, colanic acid production affected the initial interaction in a substrate-dependent manner, but the subsequent stage of biofilm development, stable adhesion, over production of colanic acid inhibited adhesion to all the surfaces tested. For the later stages of biofilm formation, colanic acid production did not appear to be required for biofilm formation since the absence of colanic acid production did not prevent biofilm formation. However, over production of colanic acid was observed to promote biofilm formation at later time points despite inhibiting the initial stage of biofilm formation, bacterial adhesion. In addition, differences in the presence of colanic acid caused architectural changes in the biofilm, indicating that colanic acid production is not required for biofilm formation for E. coli, but does play a role in modulating biofilm architecture.;The regulation of colanic acid synthesis during biofilm formation was evaluated by examining the effect of gene disruptions in the Rcs ( Regulator of Capsule Synthesis) signal transduction pathway. Specifically, rcsF, rcsC, and rcsA mutants were evaluated for their role in biofilm development and architecture. The unstable positive regulator RcsA was found to be dispensable for biofilm formation. However, loss of the upstream regulators RcsF and RcsC resulted in biofilm architectural changes distinct from those observed for the lack of colanic acid production. This suggests that deletion of the upstream regulators rcsC and rcsF may be affecting biofilm architectural through downstream targets or due to membrane perturbations due to the absence of an outer membrane lipoprotein or inner membrane protein. |
