Transmissible Gastroenteritis Virus Infection Up-Regulates FcRn Expression via Nucleocapsid Protein and Secretion of TGF-ß in Porcine Intestinal Epithelial Cells

Qian, Shaoju; Gao, Zitong; Cao, Rui; Yang, Kang; Cui, Yijie; Li, Shaowen; Meng, Xianrong; He, Qigai; Li, Zili

Transmissible gastroenteritis virus infection up-regulates the expression levels of IL-1β, IL-6, IL-8, TNF-α, and TGF-β, which are important factors in chronic inflammation. The expression of FcRn was up-regulated by the inflammatory cytokine TNF-α and IL-1β in a dose-dependent manner, as determined by RT-qPCR (Figures 3A,B) , and this was consistent with that observed in a previous study (Liu et al., 2007) . MAPK is a highly conserved serine protein kinase in the cytoplasm that mediates a signaling pathway that plays an important role in the body's inflammatory response. The MAPK family is mainly divided into three classes: extracellular signal-regulated kinases (ERKs), JNKs, and p38 MAPK kinases. Multiple stimulating factors activate the MAPK pathway, including inflammatory factors, growth factors, and cellular responses (Huang et al., 2004) . TGF-β dose-dependently induces pIgR production via the p38/MAPK pathway in human bronchial epithelial cells (Ratajczak et al., 2010) . Moreover, TGFβ was said to inhibit pIgR production in bronchial epithelium (Gohy et al., 2014) . In this study, we observed that TGF-β upregulates FcRn via the JNK MAPK pathway, perhaps because TGEV activates the JNK MAPK pathway in porcine cells.