Identification of Nuclear Factor-B Pathway Genes in Chicken Erythrocytes and their Expression Level in Erythrocytes after Infection with Mycoplasma synoviae

Mycoplasma synoviae is one of the most important pathogens in the poultry industry and often causes diseases of a chronic and persistent nature. However, there is limited data available on Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B) signaling pathway genes expression in chicken erythrocytes infected with Mycoplasma synoviae (M. synoviae). Therefore, the aim of the current in-vitro study was to determine the interaction between chicken erythrocytes and M. synoviae using Transmission electron microscope (TEM) and further to investigate the mRNA gene expression of MyD88 (Myeloid differentiation primary response 88), CCL5 (C-C Motif Chemokine Ligand 5), MDA5 (melanoma differentiation-associated protein 5) IKBKE (inhibitor of nuclear factor kappa-B kinase subunit epsilon), NFKBIA (NF-kappa-B inhibitor alpha), NFKBIE (NF-kappa-B inhibitor epsilon), Interferon Alpha (IFN-alpha), cMGF (chicken myelomonocytic growth factor), and TRAF6 (Tumor necrosis factor receptor-associated factor 6) in chicken erythrocytes infected with M. synoviae using quantitative real-time PCR (qRT-PCR) at four different time intervals (0, 2, 6 and 10 h) post-infection and compared to uninfected controls. The results indicated that M.synoviae interacted efficiently in chicken erythrocytes, which strongly induced the up-regulation of NF-kappa B pathway and other immune system genes in response to early bacterial infection such as NFKBIA, NFKBIE, IKBKE, CCL5, MDA5, MyD88, and TRAF6 at different h's interval. Whereas cMGF and IFN-alpha expression were significantly downregulated during early time intervals such as 0 h, 2 h and 6 h while later on the expression level significantly increased. These results will lead to increased insights on M. synoviae infection resistance mechanisms and the role of NF-kappa B signaling pathway and other immune system genes in the control of the host immune response.