Regulation of chicken immunity-related genes and host response profiles against Avibacterium paragallinarum pathogen challenge.

Vet Immunol Immunopathol

Faculty of Natural and Agricultural Science, Department of Microbial, Biochemical and Food Biotechnology, University of the Free State, P.O Box 339, Bloemfontein, 9300, South Africa.

Published: September 2015

AI Article Synopsis

  • Infectious coryza (IC) is a respiratory disease in chickens caused by Avibacterium paragallinarum, and this study focused on understanding the immune response in infected chickens.
  • Gene expression profiling of 30 genes was performed on nasal samples from 11 chickens, including a control group, using real-time PCR for analysis.
  • The findings indicated that the immune response is triggered by TLR4, leading to a Th2-dominant response and early production of inflammatory cytokines through the MyD88-dependent signaling pathway.

Article Abstract

Infectious coryza (IC) is a well-recognised and commonly encountered upper respiratory tract disease in chickens. The aim of this study was to monitor aspects of the immune response of chickens infected with Avibacterium paragallinarum. Gene expression profiling of 30 genes was carried out for 11 chicken nasal area samples belonging to four groups, including one non-infected control group. For this purpose, 30 biomarker transcripts were selected for comparative gene expression analysis and were analysed by real-time PCR using TaqMan(®) assays. The biomarkers included three reference genes. The reference genes were used to normalise the results in a relative quantification approach. The gene expression changes of the 27 biomarker transcripts (genes of interest) were quantified between all treated groups in six pair-wise comparisons. It was concluded from the data that immune response initiation is via TLR4, which leads to a Th2 dominant type response. Furthermore, TLR4 results in signalling via the MyD88-dependent pathway, resulting in early onset of NF-kβ leading to the production of inflammatory cytokines. This work provides an informative outlay of immune response initiation upon infection with this pathogen.

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Source
http://dx.doi.org/10.1016/j.vetimm.2015.06.005DOI Listing

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