Use of bacterial culture supernatants as anti-biofilm agents against Pseudomonas aeruginosa and Klebsiella pneumoniae.

OBJECTIVE: Pseudomonas aeruginosa and Klebsiella pneumoniae are the most pervasive and challenging agents of bacterial nosocomial infections. Previous studies indicated that the microbial biofilms formed by these bacteria may play important roles in their pathogenesis and resistance to phagocytosis and antibiotics. The aim of this study was to explore the anti-biofilm activity of culture supernatants of Salmonella enterica subsp. enteric serovar Typhimurium SL1344 and P. aeruginosa PA01 against biofilms formed by P. aeruginosa PA01 and K. pneumoniae KR3167, respectively. MATERIALS AND METHODS: Biofilm formation was quantified by crystal violet staining. A modified method was applied to separate planktonic and biofilm-forming cells. The viable cells in the planktonic and biofilm phases were quantitated by viable plate count. Dual-species interactions between P. aeruginosa PAO1 and Salmonella enterica subsp. enterica serovar Typhimurium SL1344 were investigated using different cell density ratios. RESULTS: Biofilm formation of P. aeruginosa PA01 was significantly inhibited by the heat resistant components from the culture supernatants of Salmonella enterica subsp. enterica serovar Typhimurium. Biofilm formed by K. pneumoniae KR3167 was also inhibited by the culture supernatants of P. aeruginosa PA01. The supernatants obtained from planktonic cell caused greater biofilm reduction than those extracted from biofilm-forming cells. CONCLUSIONS: This study is the first to report that sterile crude supernatants extracted from the cultures of Salmonella enterica and P. aeruginosa significantly inhibited biofilm formation of P. aeruginosa and K. pneumoniae, respectively. The active agents in the culture supernatants responsible for biofilm inhibition have not been determined yet. The culture supernatants of Salmonella enterica and P. aeruginosa should be further studied for their therapeutic potential to reduce biofilm formation produced by bacteria causing nosocomial infections.