Biofilm formation results in medical threats or economic losses and is therefore a major concern in a variety of domains. In two-species biofilms of marine bacteria grown under dynamic conditions, Pseudoalteromonas sp. strain 3J6 formed mixed biofilms with Bacillus sp. strain 4J6 but was largely predominant over Paracoccus sp. strain 4M6 and Vibrio sp. strain D01. The supernatant of Pseudoalteromonas sp. 3J6 liquid culture (SN 3J6 ) was devoid of antibacterial activity against free-living Paracoccus sp. 4M6 and Vibrio sp. D01 cells, but it impaired their ability to grow as single-species biofilms and led to higher percentages of nonviable cells in 48-h biofilms. Antibiofilm molecules of SN 3J6 were able to coat the glass surfaces used to grow biofilms and reduced bacterial attachment about 2-fold, which might partly explain the biofilm formation defect but not the loss of cell viability. SN 3J6 had a wide spectrum of activity since it affected all Gram-negative marine strains tested except other Pseudoalteromonas strains. Biofilm biovolumes of the sensitive strains were reduced 3-to 530-fold, and the percentages of nonviable cells were increased 3-to 225-fold. Interestingly, SN 3J6 also impaired biofilm formation by three strains belonging to the human-pathogenic species Pseudomonas aeruginosa, Salmonella enterica, and Escherichia coli. Such an antibiofilm activity is original and opens up a variety of applications for Pseudoalteromonas sp. 3J6 and/or its active exoproducts in biofilm prevention strategies.Biofilms are defined as microbial communities of cells that are irreversibly attached to a substratum, to an interface, or to each other and are embedded into a matrix of extracellular polymeric substances that they have produced (8). It is now considered that most (if not all) bacteria are capable of forming biofilms and that this is their predominant bacterial lifestyle. Biofilm formation is a complex biological phenomenon and has been generally described as a temporal process involving a succession of distinct stages: a reversible and then irreversible attachment of planktonic bacteria onto a surface, the formation of microcolonies either by the clonal growth of attached cells or by the active translocation of cells across the surface, the coalescence of growing microcolonies to form a macrocolony, and cell dispersal. It should, however, be noted that this developmental model still requires further experimental validation, especially concerning the possibility of a hierarchical order of genetic pathways (26). Furthermore, Karatan and Watnick (17) pointed out that there are as many different types of biofilms as there are bacteria and that a single bacterium may even make several different types of biofilms under different environmental conditions. Biofilm formation is associated with the virulence of pathogenic bacteria, and cells included within a biofilm are generally more resistant (up to 1,000-fold) to antibiotics and disinfectants than free-living bacteria (8,26). Biofilms are therefore a major concern...

The extracytoplasmic function sigma factor AlgU of Pseudomonas aeruginosa is responsible for alginate overproduction, leading to mucoidy and chronic infections of cystic fibrosis patients. We investigated here the role of AlgU in the formation of nonmucoid biofilms. The algU mutant of P. aeruginosa PAO1 (PAOU) showed a dramatic impairment in biofilm formation under dynamic conditions. PAOU was defective both in cell attachment to glass and in development of robust, shear-resistant biofilms. This was explained by an impaired production of extracellular matrix, specifically of the exopolysaccharide Psl, as revealed by microscopy and enzyme-linked immunosorbent assay. Complementing the algU mutation with a plasmid-borne algU gene restored wild-type phenotypes. Compared with that in PAO1, expression of the psl operon was reduced in the PAOU strain, and the biofilm formation ability of this strain was partially restored by inducing the transcription of the psl operon. Furthermore, expression of the lectin-encoding lecA and lecB genes was reduced in the PAOU strain. In agreement with the requirement of LecB for type IV pilus biogenesis, PAOU displayed impaired twitching motility. Collectively, these genetic downregulation events explain the biofilm formation defect of the PAOU mutant. Promoter mapping indicated that AlgU is probably not directly responsible for transcription of the psl operon and the lec genes, but AlgU is involved in the expression of the ppyR gene, whose product was reported to positively control psl expression. Expressing the ppyR gene in PAOU partially restored the formation of robust biofilms.

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