Biofilm Formation, Motility, and Virulence of Are Reduced by Deletion of the Gene , a Novel Listerial LPXTG Surface Protein.

Listeria monocytogenes () is a foodborne pathogen that causes listeriosis in humans and other animals. Surface proteins with the LPXTG motif have important roles in the virulence of . Lmo0159 is one such protein, but little is known about its role in virulence, motility, and biofilm formation. Here, we constructed and characterized a deletion mutant of (∆). We analyzed not only the capacity of biofilm formation, motility, attachment, and intracellular growth in different cell types but also LD; bacterial load in mice's liver, spleen, and brain; expression of virulence genes; and survival time of mice after challenge. The results showed that the cross-linking density of the biofilm of ∆ strain was lower than that of WT by microscopic examination. The expression of biofilm-formation and virulence genes also decreased in the biofilm state. Subsequently, the growth and motility of ∆ in the culture medium were enhanced. Conversely, the growth and motility of were attenuated by ∆ at both the cellular and mouse levels. At the cellular level, ∆ reduced plaque size; accelerated scratch healing; and attenuated the efficiency of adhesion, invasion, and intracellular proliferation in swine intestinal epithelial cells (SIEC), RAW264.7, mouse-brain microvascular endothelial cells (mBMEC), and human-brain microvascular endothelial cells (hCMEC/D3). The expression of virulence genes was also inhibited. At the mouse level, the LD of the ∆ strain was 10 times higher than that of the WT strain. The bacterial load of the ∆ strain in the liver and spleen was lower than that of the WT strain. In a mouse model of intraperitoneal infection, the deletion of the gene significantly prolonged the survival time of the mice, suggesting that the deletion mutant also exhibited reduced virulence. Thus, our study identified as a novel virulence factor among LPXTG proteins.