Abstract
Biofilm formation is an integral part of the microbial life cycle in nature. In food processing environments, bacterial transmissions occur primarily through raw or undercooked foods and by cross-contamination during unsanitary food preparation practices. Foodborne pathogens form biofilms as a survival strategy in various unfavorable environments, which also become a frequent source of recurrent contamination and outbreaks of foodborne illness. Instead of focusing on bacterial biofilm formation and their pathogenicity individually, this review discusses on a molecular level how these two physiological processes are connected in several common foodborne pathogens such as Listeria monocytogenes, Staphylococcus aureus, Salmonella enterica and Escherichia coli. In addition, biofilm formation by Pseudomonas aeruginosa is discussed because it aids the persistence of many foodborne pathogens forming polymicrobial biofilms on food contact surfaces, thus significantly elevating food safety and public health concerns. Furthermore, in-depth analyses of several bacterial molecules with dual functions in biofilm formation and pathogenicity are highlighted.
Highlights
Bacterial Biofilms and Food Safety ConcernsMost microbes found in nature exist in biofilms, a well-structured, dynamic, diverse, synergistic and protective microbial community [1,2]
This study reported that the PrfA regulated InlA, InlB, and Listeriolysin O (LLO) were neither involved in bacterial sedimentation nor aggregation [75], and ruled out their involvement in biofilm formation
These findings suggest that biofilms produced by Pseudomonas provide a shelter for foodborne pathogens for persistence and product contamination, and indirectly jeopardizes the safety of food products
Summary
Most microbes found in nature exist in biofilms, a well-structured, dynamic, diverse, synergistic and protective microbial community [1,2]. PrfA positively impacts the extracellular environment and mutants lacking prfA are defective in surface-adhered biofilm formation [71] possibly due to the impaired regulatory response of key aggregation factors (see below) Both virulence gene regulators and virulence factors are shown to be involved in biofilm formation in L. monocytogenes (Table 2). Though ActA is involved in the host cell cytoskeletal rearrangement to propel L. monocytogenes in the cytosol, it is reported to be involved in bacterial aggregation and biofilm formation [75]. ActA is responsible for a sedimentation phenotype, which is essential for bacterial aggregation and biofilm formation These phenotypes were significantly reduced or absent in strains with deleted prfA or actA gene which was verified both in vitro cell culture and in vivo animal models (Table 2). This study reported that the PrfA regulated InlA, InlB, and LLO were neither involved in bacterial sedimentation nor aggregation [75], and ruled out their involvement in biofilm formation
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