Pseudomonas aeruginosa is a major cause of opportunistic infections. P. aeruginosa is found in an estimated 10-20% of all hospital acquired infections; it is implicated in respiratory infections, urinary tract infections, gastrointestinal infections, keratitis, otitis media, and bacteremia. It is also the predominant cause of morbidity and mortality in cystic fibrosis patients, whose abnormal airway epithelia allow a chronic long-term colonisation of the lungs. Chronic infections such as this are characterised by the formation of a biofilm. Biofilms are a community of cells encased in an extracellular matrix consisting of secreted proteins, polysaccharides and nucleic acids attached to surfaces. Bacteria within biofilms are more resistant to antibiotics, dynamic forces and host defences. With the realisation that biofilms are of substantive importance to infectious diseases, it has become crucial to understand the mechanisms that govern biofilm development and the role of biofilms in bacterial pathogenesis in order to develop new therapies to treat these infections. Many proteins of the autotransporter (AT) class of secreted protein from Gram-negative bacteria have been found to be involved in biofilm formation. All AT proteins possess some common features: an N-terminal signal sequence, a passenger domain that is secreted to the cell surface and a translocation domain that forms a β-barrel pore that assists the passenger domain in gaining access to the surface. The passenger domain is responsible for the function of the AT protein. Using a bioinformatic approach Dr Wells has identified a further four distinct AT proteins in the five P. aeruginosa genomes available. The aim of this project is to utilise Dr. Wells’ substantial experience with E. coli autotransporters in order to study the role of autotransporter proteins in the virulence, colonisation and biofilm formation of Pseudomonas aeruginosa especially in regard to cystic fibrosis infections.