Models and mechanisms for bacteriocin action and application

There is considerable research on bacteriocin genetics, purification, and properties. Less is known about the mechanism(s) by which bacteriocins kill pathogens, the physical chemistry of the bacteriocin/pathogen interaction, and of the variables which influence bacteriocins' efficacy in foods. Such knowledge is prerequisite to the wider applications of bacteriocins and to increasing their efficacy by genetic engineering. Mechanistic studies using spores as bacteriocin targets are relatively few. Empirical challenge studies in a variety of foods have had mixed results. Working with well defined model foods, we have determined that increasing protein or phospholipid concentrations decrease nisin's effectiveness against Clostridium botulinum growth from spore inocula. Nisin is also less effective at abuse compared to refrigerated temperatures. This may be a general characteristic of bacteriocins since increasing temperature decreases many bacteriocins' inhibition of Listeria monocytogenes in foods. L. monocytogenes vegetative cells provide a better target for bacteriocin action than do C. botulinum spores. Bacteriocins dissipate proton motive force (PMF) in L. monocytogenes, C. sporogenes and vegetative cells of other sensitive species. The cytoplasmic membrane is generally considered to be the site at which bacteriocins act. We have adopted fluorescence spectroscopy to characterize the interaction of bacteriocins with liposomes comprised of lipids extracted from L. monocytogenes membranes. The regulatory status of bacteriocins, various models for bacteriocin action, and future prospects for their application are also discussed.