INTERACTIONS OF NISIN AND PEDIOCIN PA-1 WITH CLOSELY-RELATED LACTIC-ACID BACTERIA THAT MANIFEST OVER 100-FOLD DIFFERENCES IN BACTERIOCIN SENSITIVITY

Citation
Mhj. Bennik et al., INTERACTIONS OF NISIN AND PEDIOCIN PA-1 WITH CLOSELY-RELATED LACTIC-ACID BACTERIA THAT MANIFEST OVER 100-FOLD DIFFERENCES IN BACTERIOCIN SENSITIVITY, Applied and environmental microbiology, 63(9), 1997, pp. 3628-3636
Citations number
59
Categorie Soggetti
Microbiology,"Biothechnology & Applied Migrobiology
ISSN journal
00992240
Volume
63
Issue
9
Year of publication
1997
Pages
3628 - 3636
Database
ISI
SICI code
0099-2240(1997)63:9<3628:IONAPP>2.0.ZU;2-P
Abstract
The natural variation in the susceptibilities of gram positive bacteri a towards the bacteriocins nisin and pediocin PA-1 is considerable. Th is study addresses the factors associated with this variability for cl osely related lactic acid bacteria. We compared two sets of nonbacteri ocinogenic strains for which the MICs of nisin and pediocin PA-1 diffe red 100- to 1,000-fold: Lactobacillus sake DSM20017 and L. sake DSM204 97 and Pediococcus dextrinicus and Pediococcus pentosaceus. Strikingly , the bacteriocin-sensitive and -insensitive strains showed a similar concentration-dependent dissipation of their membrane potential (Delta Psi) after exposure to these bacteriocins. The bacteriocin-induced di ssipation of Delta Psi below the MICs far the insensitive strains did not coincide with a reduction of intracellular ATP pools and glycolyti c rates. This was not observed with the sensitive strains. Analysis of membrane lipid properties revealed minor differences in the phospho-a nd glycolipid compositions of both sets of strains. The interactions o f the bacteriocins with strain specific lipids were not significantly different in a lipid monolayer assay. Further lipid analysis revealed higher in situ membrane fluidity of the bacteriocin-sensitive Pediococ cus strain compared with that far the insensitive strain, but the oppo site was found for the L. sake strains. Our results provide evidence t hat the association of bacteriocins with the cell membrane and their s ubsequent insertion take place in a similar way for cells that have a high or a low natural tolerance towards bacteriocins. Far insensitive strains, overall membrane constitution rather than mere membrane fluid ity may preclude the formation of pores with sufficient diameters and lifetimes to ultimately cause cell death.