Background: Internalins are surface proteins that are utilized by Listeria monocytogenes to facilitate its invasion into human intestinal epithelial cells. The expression of a full-length InlA is one of essential virulence factors for L. monocytogenes to cross the intestinal barrier in order to invade epithelial cells.
Results: In this study, the gene sequences of inlA in 120 L. monocytogenes isolates from food (n = 107) and humans (n = 13) were analyzed. Premature stop codon (PMSC) mutations in inlA were identified in 51 isolates (50 from food and 1 from human). Six mutation types of PMSCs were identified. Among the 51 isolates with PMSCs in inlA, there were 44 serogroup 1/2c, 3c isolates from food, of which seven belonged to serogroups 1/2a, 3a. A total of 153,382 SNPs in 2247 core genes from 42 genomes were identified and used to construct a phylogenetic tree. Serotype 1/2c isolates with inlA PMSC mutations were grouped together. Cell culture studies on 21 isolates showed that the invasion to Caco-2 cells was significantly reduced among isolates with inlA PMSC mutations compared to those without PMSC mutations (P < 0.01). The PMSC mutations in inlA correlated with the inability of the L. monocytogenes isolates to invade Caco-2 cells (Pearson's coefficient 0.927, P < 0.01).
Conclusion: Overall, the study has revealed the reduced ability of L. monocytogenes to invade human intestinal epithelial cells in vitro was linked to the presence of PMSC mutations in inlA. Isolates with PMSC mutations shared the same genomic characteristics indicating the genetic basis on the potential virulence of L. monocytogenes invasion.
Keywords: Internalins; Invasion; L. monocytogenes; PMSC mutation; inlA.