The intracellular bacterial pathogen Listeria monocytogenes can breach protective barriers in the pregnant host, allowing the colonization of the placenta in pregnant people and resulting in numerous adverse pregnancy outcomes. Previous studies aimed at delineating the mechanisms behind placental colonization of L. monocytogenes identified a key virulence factor, internalin P (InlP). The internalin family of proteins has been studied extensively due to their conservation in the genus Listeria and their contribution to virulence and pathogenicity in L. monocytogenes. Still, many questions remain regarding the evolution of internalins and their potential roles in non-pathogenic Listeria. Our work addresses this gap in knowledge by (1) identifying additional InlP homologs in Listeria, including L. ivanovii, L. seeligeri, L. innocua, and L. costaricensis, and (2) characterizing these homologs using computational evolutionary methods to compare their primary sequences, domain architectures, and structural models. Together, our findings contribute to the field by providing insights into the evolution of one key member of the internalin family, as well as serving as a catalyst for future studies of InlP and its role in Listeria pathogenesis.