Impact of fliD and virulence plasmid pSEV on response of chicken embryo fibroblasts to Salmonella Enteritidis
Language English Country Netherlands Media print-electronic
Document type Journal Article
PubMed
29695318
DOI
10.1016/j.vetimm.2017.12.003
PII: S0165-2427(17)30299-4
Knihovny.cz E-resources
- Keywords
- CEF gene expression, ENO2, G0S2, Salmonella virulence, fliD, pSEV,
- MeSH
- Bacterial Proteins genetics MeSH
- Fibroblasts microbiology MeSH
- Flagella genetics MeSH
- Host-Pathogen Interactions MeSH
- Chick Embryo MeSH
- Real-Time Polymerase Chain Reaction MeSH
- Poultry Diseases immunology microbiology MeSH
- Plasmids genetics MeSH
- Salmonella enteritidis genetics pathogenicity MeSH
- Salmonella Infections, Animal immunology microbiology MeSH
- Virulence genetics MeSH
- Animals MeSH
- Check Tag
- Chick Embryo MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Bacterial Proteins MeSH
- FlaD protein, Bacteria MeSH Browser
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.
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