Bacterial biofilms

Abstract

Many bacteria have evolved specialized mechanisms to adhere to solid surfaces by forming glycocalyx-enriched biofilms. Pseudomonas aeruginosa can form biofilms on medical indwelling devices and in the lungs of most cystic fibrosis patients. Crucial to understanding biofilm structure and maintenance is deciphering how cells communicate within this complex community. Two cell–cell signalling systems, LasR/LasI and RhlR/RhlI (VsmR/VsmI), have been identified in P. aeruginosa. Why P. aeruginosa requires two such systems and the role(s) of each of these systems have been the subject of intense research in recent years. Davies et al.[ 1 Davies D.C. et al. The involvement of cell-to-cell signals in the development of a bacterial biofilm. Science. 1998; 280: 295-298 Crossref PubMed Scopus (2529) Google Scholar ]now report that LasI, which directs the synthesis of a diffusible extracellular signal [N-(3-oxododecanoyl)-l-homoserine lactone (3OC12HSL)], plays a key role in the maintenance of P. aeruginosa biofilms. A lasI mutant formed a uniformly thin surface layer in contrast to the thick biofilms formed by an rhlI mutant and the wild-type strain. In the presence of 3OC12-HSL, the lasI biofilm was restored to normal cell density and thickness. In addition, the abnormal lasI biofilm was dispersed by exposure to 0.2% SDS, whereas a similar treatment had no detectable effect on the wild-type biofilm. Bacterial biofilms of mixed and individual species present significant economic problems in industry and medicine. Strategies designed to inhibit bacterial cell–cell signalling could aid in the control and eradication of unwanted biofilms.