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Characterization of internalin genes in Listeria monocytogenes from food and humans, and their association with the invasion of Caco-2 cells.
Gut Pathogens ( IF 4.3 ) Pub Date : 2019-06-10 , DOI: 10.1186/s13099-019-0307-8
Xudong Su 1 , Guojie Cao 2 , Jianmin Zhang 1 , Haijian Pan 1 , Daofeng Zhang 1 , Dai Kuang 1 , Xiaowei Yang 1 , Xuebin Xu 3 , Xianming Shi 1 , Jianghong Meng 2
Affiliation  

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.

中文翻译:

来自食物和人类的单核细胞增生李斯特菌内蛋白基因的表征,以及它们与 Caco-2 细胞入侵的关联。

背景 内蛋白是单核细胞增生李斯特菌用来促进其侵入人体肠上皮细胞的表面蛋白。全长InlA的表达是单核细胞增生李斯特菌穿过肠道屏障以侵入上皮细胞的重要毒力因子之一。结果本研究分析了120株来自食物(n = 107)和人类(n = 13)的单核细胞增生李斯特菌的inlA基因序列。在 51 个分离株(50 个来自食物和 1 个来自人类)中鉴定了 inlA 中的过早终止密码子 (PMSC) 突变。鉴定了六种突变类型的 PMSC。在inlA的51株PMSCs中,从食物中分离出1/2c、3c血清群44株,其中1/2a、3a血清群7株。一共153个,鉴定了来自 42 个基因组的 2247 个核心基因中的 382 个 SNP,并用于构建系统发育树。具有 inlA PMSC 突变的血清型 1/2c 分离株被归为一组。对 21 个分离株的细胞培养研究表明,与没有 PMSC 突变的分离株相比,具有 inlA PMSC 突变的分离株对 Caco-2 细胞的侵袭显着降低(P < 0.01)。inlA 中的 PMSC 突变与 L. monocytogenes 分离株不能侵入 Caco-2 细胞相关(皮尔逊系数 0.927,P < 0.01)。结论 总体而言,该研究表明,单核细胞增生李斯特菌在体外侵入人肠上皮细胞的能力降低与 inlA 中 PMSC 突变的存在有关。具有 PMSC 突变的分离株具有相同的基因组特征,表明 L.
更新日期:2020-04-22
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