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fliD和毒力质粒pSEV对鸡胚成纤维细胞对肠炎沙门氏菌反应的影响。

Impact of fliD and virulence plasmid pSEV on response of chicken embryo fibroblasts to Salmonella Enteritidis.

作者信息

Szmolka Ama, Matulova Marta Elsheimer, Rychlik Ivan

机构信息

Institute for Veterinary Medical Research, Centre for Agricultural Research, Hungarian Academy of Sciences, Hungária krt. 21, 1143 Budapest, Hungary.

Veterinary Research Institute, Hudcova 70, 621 00, Brno, Czech Republic.

出版信息

Vet Immunol Immunopathol. 2018 Feb;196:1-4. doi: 10.1016/j.vetimm.2017.12.003. Epub 2017 Dec 6.

DOI:10.1016/j.vetimm.2017.12.003
PMID:29695318
Abstract

Salmonella Enteritidis is the main serovar of poultry origin in humans, but its complex interaction with certain avian cells is still not fully understood. Previously we identified several genes significantly induced in chicken embryo fibroblasts (CEFs) by the wild-type strain S. Enteritidis 11 (SE 11). In the present study, we raised the question whether virulence-attenuated mutants of this strain would induce altered expression of the newly identified fibroblast genes associated with immune and non-immune functions of CEFs. Gene expression was evaluated by real-time PCR following challenge by the parental strain SE 11 and its virulence attenuated mutants lacking flagellin gene fliD only or fliD and the serovar-specific virulence plasmid pSEV. As a result, deletion mutants induced a lower expression of all immune genes, but an increased expression of the non-immune genes G0S2 and ENO2 relative to the parental strain. Our data indicate the importance of flagella and pSEV in modulation of virulence and host response in this model. We demonstrated, for the first time ever, an increased induction of survival genes G0S2 and ENO2 by virulence-attenuated mutants of S. Enteritidis.

摘要

肠炎沙门氏菌是人类中源自家禽的主要血清型,但其与某些禽类细胞的复杂相互作用仍未完全了解。此前,我们鉴定出野生型肠炎沙门氏菌11株(SE 11)在鸡胚成纤维细胞(CEF)中显著诱导表达的几个基因。在本研究中,我们提出一个问题,即该菌株的减毒毒力突变体是否会诱导与CEF免疫和非免疫功能相关的新鉴定成纤维细胞基因表达发生改变。在用亲本菌株SE 11及其仅缺失鞭毛蛋白基因fliD或同时缺失fliD和血清型特异性毒力质粒pSEV的减毒毒力突变体进行攻击后,通过实时PCR评估基因表达。结果,与亲本菌株相比,缺失突变体诱导所有免疫基因的表达降低,但非免疫基因G0S2和ENO2的表达增加。我们的数据表明鞭毛和pSEV在该模型中对毒力调节和宿主反应的重要性。我们首次证明肠炎沙门氏菌的减毒毒力突变体对存活基因G0S2和ENO2的诱导增加。

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