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Biofilm formation in the uropathogenic Escherichia coli strain CFT073: identification of cryptic adhesion factors

Final Activity Report Summary - CRYPTIC-UROBIOFILMS (Biofilm formation in the uropathogenic Escherichia coli strain CFT073: identification of cryptic adhesion factors)

Uropathogenic strains of Escherichia coli (UPEC), which colonise and persist in the urinary tract, are the most common cause of non-hospital-acquired urinary tract infections. One of the major factors associated with the virulence of UPEC is their ability to form biofilms. Biofilm-like structures generally provide a protective environment for their constituent bacteria, shielding them form antibiotics and host effects. Adhesins are the major factors associated with virulence of UPEC, which mediate specific attachment to host receptors and trigger innate host responses. The biological significance of both of the potential adhesins and their role in UPEC pathogenesis has been investigated. We have performed a detailed molecular characterisation of Ag43a, Ag43b and UpaG and showed that the expression of Ag43a, Ag43b and UpaG revealed that they possess different functional properties. Ag43a and UpaG produced a strong aggregation phenotype and promoted significant biofilm growth. When these mutants were analysed in a mouse model of UTI, Ag43a (but not Ag43b) promoted long-term persistence in the urinary bladder. Our findings reveal the existence of pathogenicity-adapted variants of Ag43 with distinct virulence-related functions.

Urinary tract infections occur as a continuum where initially, uropathogenic strains of Escherichia coli entry via the oral route and progress through the intestine where they habit as commensal bacteria until they cross to the urinary tract. The capacity of uropathogenic Escherichia coli to interact with bacterial communities encountered in the intestinal environment is a poorly known step in the infection process. In order to study UPEC interactions with multicellular biofilm bacterial communities, we developed an in vitro mixed bacterial model in microfermentors. We demonstrate here that the UPEC strain CFT073 as well as all E. coli expressing group II capsule, release into their environment a soluble polysaccharide that induces physico-chemical surface alterations which prevent biofilm formation by a wide range of Gram-positive and Gram-negative bacteria. We show that the treatment of abiotic surfaces with group II capsular polysaccharides drastically reduces both initial adhesion and biofilm development by important nosocomial pathogens. These findings identify capsular polymers as anti-adhesion bacterial interference molecules, which may prove to be of significance in the design of new strategies to limit biofilm formation on medical indwelling devices.