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 bacterio cins kill pathogens, the physical chemistry of the bacteriocin/pathoge n interaction, and of the variables which influence bacteriocins' effi cacy in foods. Such knowledge is prerequisite to the wider application s of bacteriocins and to increasing their efficacy by genetic engineer ing. Mechanistic studies using spores as bacteriocin targets are relat ively few. Empirical challenge studies in a variety of foods have had mixed results. Working with well defined model foods, we have determin ed that increasing protein or phospholipid concentrations decrease nis in's effectiveness against Clostridium botulinum growth from spore ino cula. Nisin is also less effective at abuse compared to refrigerated t emperatures. This may be a general characteristic of bacteriocins sinc e increasing temperature decreases many bacteriocins' inhibition of Li steria monocytogenes in foods. L. monocytogenes vegetative cells provi de 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 cy toplasmic membrane is generally considered to be the site at which bac teriocins act. We have adopted fluorescence spectroscopy to characteri ze the interaction of bacteriocins with liposomes comprised of lipids extracted from L. monocytogenes membranes. The regulatory status of ba cteriocins, various models for bacteriocin action, and future prospect s for their application are also discussed.