A novel cell wall-anchored peptidoglycan hydrolase (autolysin), IspC, essential for Listeria monocytogenes virulence: genetic and proteomic analysis

Pathogens Penetrating the Central Nervous System: Infection Pathways and the Cellular and Molecular Mechanisms of Invasion

“…However, in intravenously inoculated mice, the ⌬vip strain was attenuated for virulence and associated with a significant decrease in bacterial loads within the brain (160). Similarly, IspC was also shown to contribute to L. monocytogenes invasion of the brain in a mouse model of hematogenous meningitis (233). Interestingly, the deletion of IspC did not affect the ability of L. monocytogenes to attach to and invade HBMECs in vitro.…”

“…In contrast, the ⌬ispC strain demonstrated a significant reduction in attachment and invasion in sheep choroid plexus epithelial cells (compared to wild-type L. monocytogenes), and purified IspC was capable of binding to these cells. Proteomic analyses revealed that IspC regulates the expression of other virulence factors, including ActA, InlC2, and a flagellin homologue (FlaA); therefore, the phenotype observed for the ⌬ispC strain may be a result of the deletion of IspC in combination with a reduction in the expression of these factors (233).…”

Entry of Listeria monocytogenes in Mammalian Epithelial Cells: An Updated View

“…Ami, a N-acetylmuramoyl-L-alanine amidase ) is required for adhesion but not for invasion of host cells in an DinlA, DinlB, or DinlAB background only (Milohanic et al 2000), and interestingly, the eight GW repeats of Ami are sufficient to promote L. monocytogenes adhesion to host cells (Milohanic et al 2001). Auto, the only L. monocytogenes autolysin absent from the genome of L. innocua, is required for invasion (not adhesion) to several mammalian cell lines ), whereas IspC is required for bacterial adhesion and/or invasion in a cell line-dependent manner (Wang and Lin 2008). Intriguingly, the Dami, Dauto, and DispC strains do not display major morphological abnormalities (ActA surface expression is only affected in the DispC mutant) suggesting that these molecules probably play a minor role as autolysins in vitro; their importance is highlighted by the reduced virulence of the mutant strains in the mouse model in vivo.…”

CwpFM (EntFM) Is a Bacillus cereus Potential Cell Wall Peptidase Implicated in Adhesion, Biofilm Formation, and Virulence

“…Many of theses proteins display, in addition to their catalytic site, a domain necessary for the interaction with peptides, carbohydrates, and lipids of the cell wall, such as SH3, LysM, and the peptidoglycan binding domain. Bacterial cell wall peptidases are involved in various processes, such as peptidoglycan modification during growth, cell wall turnover, separation of daughter cells during cell division, motility, bacterial adhesion and invasiveness, and biofilm formation, and therefore contribute directly to bacterial pathogenicity (10,23,28,38,43,45,47). EntFM was first named an enterotoxin, but BLAST and secondary structure analyses revealed similarity to cell wall peptidases of the NlpC/P60 family.…”