Effect of 25-hydroxyvitamin D-3 on rotavirus replication and gene expressions of RIG-I signalling molecule in porcine rotavirus-infected IPEC-J2 cells

摘要

The study evaluated whether a 25-hydroxyvitamin D-3 (25D(3)) supplementation decreases the replication of rotavirus by the retinoic acid-inducible gene I (RIG-I) signalling pathway in a porcine small intestinal epithelial cell line (IPEC-J2). The results show that IPEC-J2 cells express high baseline levels of 1 alpha-hydroxylase (CYP27B1), which converts inactive 25D(3) to the active 1,25-dihydroxyvitamin D-3 (1,25D(3)). Porcine rotavirus (PRV) infection alone resulted in a significant increase in CYP27B1 mRNA, which augmented the production of active vitamin D. Physiological concentrations of 25D(3) were found to decrease PRV replication in IPEC-J2 cells. RIG-I plays an important role in the recognition of double-stranded RNA virus by host cells. Upon recognition, RIG-I triggers a series of signalling molecules such as interferon-beta (IFN-beta) promoter stimulator 1 (IPS-1) leading to the expression of type I interferons (IFN-beta). Active 25D(3) that was generated by PRV-infected IPEC-J2 cells led to an increased expression of toll-like receptors 3 (TLR3), RIG-I, IPS-1, IFN-beta and IFN-stimulated genes 15 (ISG(15)) with important innate immune functions. Inhibiting CYP27B1 also failed to increase RIG-I, IPS-1, IFN-beta and ISG(15) mRNA expression. These observations suggest that 25D(3) can directly inhibit PRV in IPEC-J2 cells, which requires this active form of vitamin D. The anti-rotavirus effect of 25D(3) is mediated at least in part by RIG-I signalling pathways in IPEC-J2 cells.