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Role of quorum sensing by Pseudomonas aeruginosa in microbial keratitis and cystic fibrosis

T. C. R. Conibear^1,3,

¹ School of Optometry and Vision Science, University of New South Wales, Sydney, NSW 2052, Australia
² Institute for Eye Research, Sydney, Australia
³ Vision CRC, Sydney, Australia
⁴ BioScience and Technology, The Technical University of Denmark, DK-2800 Lyngby, Denmark
⁵ School of Biotechnology and Biomolecular Sciences and The Centre for Marine Bio-Innovation, University of New South Wales, Sydney, NSW 2052, Australia

Correspondence
S. A. Rice
Scott.Rice{at}unsw.edu.au

Pseudomonas aeruginosa is a ubiquitous bacterium that causes opportunistic infections in a range of host tissues and organs. Infections by P. aeruginosa are difficult to treat and hence there is interest in the development of effective therapeutics. One of the key mechanisms that P. aeruginosa uses to control the expression of many virulence factors is the N-acylated homoserine lactone (AHL) regulatory system. Hence, there is considerable interest in targeting this regulatory pathway to develop novel therapeutics for infection control. P. aeruginosa is the principal cause of microbial keratitis and of infections in cystic fibrosis (CF) sufferers, and AHL-dependent cell-to-cell signalling has been shown to be important for both infection types. However, keratitis tends to be an acute infection whereas infection of CF patients develops into a chronic, life-long infection. Thus, it is unclear whether AHL-regulated virulence plays the same role during these infections. This review presents a comparison of the role of AHL signalling in P. aeruginosa-mediated microbial keratitis and chronic lung infections of CF patients.

Present address: School of Biological Sciences, University of Southampton, Southampton SO17 IBJ, UK.

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