Biofilms (surface-associated bacterial communities) are found in virtually every habitat. In natural and clinical setting, biofilms enhance survival, enabling organisms to adapt to changing conditions collectively instead of as single cells. It is also widely accepted that biofilms are a source of persistent infections. Bacteria are able to maintain community structure because of extracellular polymeric substances that form a matrix to enmesh bacterial cells. Exopolysaccharide is a critical biofilm matrix component. Pseudomonas aeruginosa (P. aeruginosa) can produce several biofilm matrix exopolysaccharides. However, little is known about how the synthesis of multiple exopolysaccharides is regulated.

This question is addressed in the recent discovery of Dr. MA Luyan’ group at State Key Laboratory of Microbial Resources, Institute of Microbiology, Chinese Academy of Sciences and their collaborators at the Ohio State University and University of Washington.

P. aeruginosa is an important opportunistic pathogen that can cause life-threatening persistent infections in cystic fibrosis (CF) patients and individuals with a compromised immune system. This environmental bacteriumcan produce several exopolysaccharides including alginate, Psl, and Pel, which each contribute to biofilm formation. P. aeruginosa cells often become mucoid once they have colonized the CF lung. Mucoidy is due to the overproduction of alginate that provides an advantage for P. aeruginosa in the airway of CF patients. Psl polysaccharide is a critical matrix component in nonmucoid P. aeruginosa biofilm. Dr. Ma et al. recently reported that Psl also played a key role in mucoid biofilms. Meanwhile, Dr. MA’ group discovered that the bifunctional enzyme AlgC (with phosphomannomutase and phosphoglucomutase activities) that provides sugar precursors for the synthesis of alginate and lipopolysaccharides (LPS) was also required for both Psl and Pel production.

The data suggests that the biosynthesis pathways of Psl, Pel, alginate, and LPS compete for common sugar precursors. As AlgC is the only enzyme that provides precursors for each of these exopolysaccharides, they propose that AlgC is a key checkpoint enzyme that coordinates the total amount of exopolysaccharide biosynthesis by controlling sugar precursor pool. The data also provide a plausible strategy that P. aeruginosa utilizes to modulate its biofilm matrix exopolysaccharides. These new discoveries are helpful to understand the mechanism of biofilm formation and to design therapies for biofilm-related infection.

The results were published in FEMS Immunology and Medical Microbiology (DOI:10.1111/j.1574-695X.2012.00934.x) and Environmental Microbiology ( doi:10.1111/j. 1462-2920. 2012. 02753.x).