“…Several studies have shown bacteriocin's capability in L. monocytogenes inhibition-150 AU/mL and 300 AU/mL rhamnocin 519 derived from Lactobacillus rhamnosus CJNU 0519 decreases by 0.33 log CFU/mL and no viable cells of L. monocytogenes detected at 3 h of incubation, respectively [54]; sakacin A produced by L. sakei DSMZ 6333 was shown to permeabilize Listeria cells' membrane, dissipating both transmembrane potential and transmembrane pH gradient, leading to the leakage of cellular materials [55]; pediocin PA-1 produced by P. acidilactici UL5 induced elimination of Listeria, approximately 5 log reduction within 5 h in the ileum [56]; Lactobacillus reuteri INIA P572 produces reuterin with a strong antilisterial effect [58]; 2.5 mg/L of nisin suppressed growth of L. monocytogenes for up to eight weeks in chilled conditions, and 12,800 AU/g of enterocin reduced L. monocytogenes by 1.67 log cycle in salami [59]. It is possible for Listeria to become immune to bacteriocins such as nisin (Class I bacteriocin) or Class IIa bacteriocin as reported via the production of the enzyme nisinase, which degrades nisin [29], altering the fatty acid composition, thickness, charge, or fluidity of its cell membrane [25,29,51], preventing the binding of nisin to lipid II; through a spontaneous bacteriocin resistant mutant outgrowth [42,60]; cross-resistance to other antimicrobial compounds [42,51] or other classes of bacteriocins [25,29]. Besides, the presence of genes, e.g., cell wall synthesis gene dltA and penicillin-binding protein gene lmo2229 or increased expression of β-glucoside-PTS involved in mptACD gene downregulation causing the absence of Man-PTS permease has been reported as resistant against class I and class IIa bacteriocins, respectively [25,61].…”