Bacteriocins of Listeria monocytogenes and Their Potential as a Virulence Factor

Abstract

Intestinal microbiota exerts protective effects against the infection of various bacterial pathogens, including Listeria monocytogenes, a major foodborne pathogen whose infection can lead to a disease (listeriosis) with a high fatality rate. As a strategy to mitigate the action of the intestinal microbiota, pathogens often produce antimicrobial proteinaceous compounds such as bacteriocins. In this review, we summarize the information currently available for the well-characterized L. monocytogenes bacteriocin listeriolysin S, with the emphasis on its intriguing mode of action as a virulence factor, which promotes the infection of L. monocytogenes by changing the composition of the intestinal microbiota. We then discuss another intriguing L. monocytogenes bacteriocin Lmo2776 that specifically inhibits the inflammogenic species, Prevotella copri, in the intestinal microbiota, reducing superfluous inflammation while weakening virulence. In addition, we describe relatively less studied phage tail-like Listeria bacteriocins (monocins) and elaborate on the possibility that these monocins could be involved in enhancing pathogenicity. In spite of the burgeoning interest in the roles played by the intestinal microbiota against the L. monocytogenes infection, our understanding on the virulence factors affecting the intestinal microbiota is still lacking, calling for further studies on bacteriocins that could function as novel virulence factors.

Ribosomally synthesized peptides, foreground players in microbial interactions: recent developments and unanswered questions

“…Moreover, the dehydratase/dehydrogenase LlsB encoded in the LAP operon is required for the mouse gut colonization, while listeriolysin S is not, adding another stone to the complex mechanisms of Listeria monocytogenes virulence. 239,240 Finally, another Lmo bacteriocin, Lmo2776 was shown to specifically target Prevotella copri , an abundant gut commensal, both in vivo in mouse and in vitro in reconstituted human microbiota. 241 Lmo2776 is homologous to lactococcin 972 from Lactococcus lactis , which would be an atypical unmodified bacteriocin interacting with lipid II.…”

The mobilome of Lactobacillus crispatus M247 includes two novel genetic elements: Tn7088 coding for a putative bacteriocin and the siphovirus prophage ΦM247

“…Manual homology-based annotation attributed a putative function to 14 out of 16 ORFs (). Tn 7088 has a typical IME modular organization [40] composed of (i) a mobilization module where orf3 and orf4 code for FtsK homologous proteins and orf5 for a relaxase; (ii) an integration/excision module constituted by orf7 and orf8 , coding for a putative excisionase and an integrase, respectively; and (iii) an adaptation module ( orf9 to orf16 ) homologous to the listeriolysin S ( lls ) locus of Listeria monocytogenes [41, 42] (, ). The 44 aa Orf9 is homologous to LlsA, the pro-peptide listeriolysin S family of thiazole/oxazole-modified microcins (TOMM) class I bacteriocin, and contains a 13 aa long serine/threonine/cysteine-rich motif.…”

“…Listeriolysin S biosynthesis cyclodehydratase [ 42 ], similar to L. monocytogenes LlsY, disrupted by IS Lhe5…”

Proteomic Characterization of Antibiotic Resistance in Listeria and Production of Antimicrobial and Virulence Factors

“…A total of 2990 non-redundant peptides were identified which corresponded to 2727 annotated proteins from Listeria (see complete non-redundant dataset in Excel Supplemental Data). Accordingly, the virulence factors were identified by comparison with both the "Virulence Factors of Pathogenic Bacteria Database" (VFDB; http://www.mgc.ac.cn/VFs/, accessed on 26 July 2020), and with previously reported data [1,6,10,24,25].…”

“…Escape from the host phagocytic vacuole is mediated by secreted bacterial proteins, such as PlcA, pore-forming toxin listeriolysin O (LLO), phosphatidylcholine-specific phospholipase, and phosphatidylinositol-specific phospholipase C. Intracellular actin-based motility (ActA) and cell-to-cell spread (without actual exit to the interstitial liquid) is accomplished by Hly and PlcB. All these genes are clustered into two pathogenicity islands, and the expression of the main virulence gene is controlled by transcription of the regulator PrfA, which is absent in L. innocua [ 3 , 6 , 8 , 9 , 10 , 11 ]. An additional 47 genes, scattered throughout the bacterial genome, have been identified to affect virulence [ 12 ].…”