Transcriptional Regulation of Gene by NFIB Is Associated with Cellular Immune and Inflammatory Response to APEC Infection.

Avian pathogenic (APEC) can cause localized or systemic infection, resulting in large economic losses per year, and impact health of humans. Previous studies showed that (receptor interacting serine/threonine kinase 2) and its signaling pathway played an important role in immune response against APEC infection. In this study, chicken HD11 cells were used as an in vitro model to investigate the function of chicken and the transcription factor binding to the core promoter region via gene overexpression, RNA interference, RT-qPCR, Western blotting, dual luciferase reporter assay, CHIP-PCR, CCK-8, and flow cytometry assay following APEC stimulation. Results showed that APEC stimulation promoted expression and cells apoptosis, and inhibited cells viability. Knockdown of significantly improved cell viability and suppressed the apoptosis of APEC-stimulated cells. Transcription factor NFIB (Nuclear factor I B) and GATA1 (globin transcription factor 1) binding site was identified in the core promoter region of RIP2 from -2300 bp to -1839 bp. However, only NFIB was confirmed to be bound to the core promoter of . Overexpression of exacerbated cell injuries with significant reduction in cell viability and increased cell apoptosis and inflammatory cytokines levels, whereas opposite results were observed in inhibition treatment group. Moreover, was up-regulated by overexpression, and silence mitigated the effect of overexpression in cell apoptosis, inflammation, and activation of NFκB signaling pathways. This study demonstrated that overexpression accelerated APEC-induced apoptosis and inflammation via up-regulation of mediated downstream pathways in chicken HD11 cells.