AUTHOR=Harter Eva , Lassnig Caroline , Wagner Eva Maria , Zaiser Andreas , Wagner Martin , Rychli Kathrin 

TITLE=The Novel Internalins InlP1 and InlP4 and the Internalin-Like Protein InlP3 Enhance the Pathogenicity of Listeria monocytogenes

JOURNAL=Frontiers in Microbiology

VOLUME=10

YEAR=2019

URL=https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2019.01644

DOI=10.3389/fmicb.2019.01644

ISSN=1664-302X

ABSTRACT=<p>The pathogenicity of the human foodborne pathogen <italic>Listeria monocytogenes</italic> relies on virulence factors such as internalins. In 2009/2010 two <italic>L. monocytogenes</italic> strains were responsible for a serious listeriosis outbreak in Austria, Germany, and the Czech Republic. One of these clones, QOC1, which caused 14 cases including five fatalities, encodes the novel internalins <italic>inlP1</italic>, <italic>inlPq</italic> and <italic>inlP4</italic>, and the novel internalin-like protein <italic>inlP3</italic> in the genomic region of hypervariable genetic hotspot 9 in addition to the standard set of virulence genes. The <italic>in silico</italic> prevalence study revealed that these genes rarely occur in <italic>L. monocytogenes</italic>, mainly in minor clonal complexes. To obtain first insights of the role of these genes in the pathogenicity of <italic>L. monocytogenes</italic>, we studied the gene expression under conditions mimicking the ingestion in the host. Expression of <italic>inlP1</italic>, <italic>inlP3</italic>, <italic>inlPq</italic> and <italic>inlP4</italic> was increased under gastric stress and in intracellular bacteria grown in intestinal epithelial cells. Furthermore, colonization of the liver and the spleen was slightly, but significantly reduced 72 h post infection in an oral mouse infection model when <italic>inlP1</italic> or <italic>inlP4</italic> was deleted. Moreover, the impact of InlP1 and InlP3 in virulence was shown <italic>in vitro</italic> in human intestinal epithelial cells. In this study we conclusively demonstrate a potential contribution of uncommon novel internalins and an internalin-like protein to the pathogenicity of <italic>L. monocytogenes</italic>.</p>