Harter Eva, Lassnig Caroline, Wagner Eva Maria, Zaiser Andreas, Wagner Martin, Rychli Kathrin
Department for Farm Animals and Public Health in Veterinary Medicine, Institute of Food Safety, Food Technology and Veterinary Public Health, University of Veterinary Medicine Vienna, Vienna, Austria.
Department of Biomedical Sciences, Institute of Animal Breeding and Genetics and Biomodels Austria, University of Veterinary Medicine Vienna, Vienna, Austria.
Front Microbiol. 2019 Jul 23;10:1644. doi: 10.3389/fmicb.2019.01644. eCollection 2019.
The pathogenicity of the human foodborne pathogen relies on virulence factors such as internalins. In 2009/2010 two 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 , and , and the novel internalin-like protein in the genomic region of hypervariable genetic hotspot 9 in addition to the standard set of virulence genes. The prevalence study revealed that these genes rarely occur in , mainly in minor clonal complexes. To obtain first insights of the role of these genes in the pathogenicity of , we studied the gene expression under conditions mimicking the ingestion in the host. Expression of , , and 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 or was deleted. Moreover, the impact of InlP1 and InlP3 in virulence was shown 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 .
人类食源性病原体的致病性依赖于诸如内化素等毒力因子。2009/2010年，两株菌株在奥地利、德国和捷克共和国引发了严重的李斯特菌病疫情。其中一个克隆株QOC1导致了14例病例，包括5例死亡，除了标准的毒力基因集外，它在高变基因热点9的基因组区域编码新型内化素InlP1、InlP2和新型内化素样蛋白InlP3。患病率研究表明，这些基因在该病原体中很少出现，主要存在于次要克隆复合体中。为了初步了解这些基因在该病原体致病性中的作用，我们研究了在模拟宿主摄入情况下的基因表达。在胃应激条件下以及在肠上皮细胞中生长的细胞内细菌中，InlP1、InlP2、InlP3和InlP3的表达均增加。此外，在口服小鼠感染模型中，感染72小时后，当InlP1或InlP3缺失时，肝脏和脾脏的定植略有但显著减少。此外，InlP1和InlP3在毒力方面的影响在人肠上皮细胞中得到了证实。在本研究中，我们最终证明了罕见的新型内化素和一种内化素样蛋白对该病原体致病性的潜在贡献。
