P-014. Released Exopolysaccharide (r-EPS) Produced from Lactobacillus acidophilus Reduce Biofilm Formation of Enterohemorrahgic Escherichia coli

S. Kang1, Y. Kim2, H. Yun2, S. Kim2, S. Oh1;
1Chonnam Natl. Univ., Gwangju, REPUBLIC OF KOREA, 2Korea Univ., Seoul, REPUBLIC OF KOREA.

Background: Microbial biofilms are complex communities of microorganisms that have been attached and grown on surfaces in diverse environments. In general, the biofilms are consistently resistant to antibiotics, therefore, new inhibitors with the potential to remove mature biofilms are needed. Only a few reports have focused on natural compounds that inhibit biofilm formation. To identify for natural compounds that inhibit biofilm formation, we isolated released exopolysaccharide (r-EPS) from Lactobacillus acidophilus A4 in the present study. Methods: We used bio-analytical assays include biofilm formation with crystal violet staining and continuous-flow chamber. Results: For plastic 96-well polystyrene surface that contained 1.0 mg/ml of r-EPS, the Enterohemorrahgic Escherichia coli (EHEC) O157:H7 biofilms significantly decreased by 87% compared to other components at the same concentrations as well as inhibited by 94% on a polyvinyl chloride (PVC) surface. In these studies, neither their growth rate nor their autoinducer (AI)-2 like activity were affected. In addition, initial attachment and autoaggregation of EHEC O157:H7 were inhibited by r-EPS. Interestingly, consistent reduction in biofilm formation was also observed when r-EPS was applied to the continuous-flow chamber model for 48 h. More importantly, these r-EPS could prevent biofilm formation of a wide range of Gram-negative and -positive pathogens including Salmonella enteritidis, S. Typhimurium, Yersinia enterocolitica, Pseudomonas aeruginosa, Listeria monocytogenes, and Bacillus cereus. Conclusion: This property could contribute to understanding specific mechanisms within bacterial communities and lead to the development of novel and food-grade adjuncts for microbial biofilm control.