Route of Injection Affects the Impact of InlB Internalin Domain Variants on Severity ofListeria monocytogenesInfection in Mice
The facultative intracellular pathogenListeria monocytogenescauses a severe food-borne infection in humans and animals.L. monocytogenesinvasion factor InlB interacts with the tyrosine kinase c-Met via the N-terminal internalin domain. Previously, distinct variants of the InlB internalin domain (idInlB) have been described inL. monocytogenesfield isolates. Three variants were used to restore full-length InlB expression in theL. monocytogenesstrain EGDeΔinlB. Obtained isogenicL. monocytogenesstrains were tested in the invasion assay and intravenous, intraperitoneal, and intragastric models of infection in mice. All idInlBs were functional, restored InlB activity as an invasion factor, and improved invasion of the parental strain EGDeΔinlB into human kidney HEK23 cells. Meanwhile, distinct idInlBs provided different mortality rates and bacterial loads in internal organs. When recombinant strains were compared, the variant designated idInlB14 decreased severity of disease caused by intravenous and intraperitoneal bacterial administration, whereas this variant improved intestine colonization and stimulated intragastric infection. Obtained results demonstrated that naturally occurring idInlBs differed in their impact on severity ofL. monocytogenesinfection in mice in dependence on the infection route.