title: Effect of 25-hydroxyvitamin D3 on rotavirus replication and gene expressions of RIG-I signalling molecule in porcine rotavirus-infected IPEC-J2 cells.
abstract: The study evaluated whether a 25-hydroxyvitamin D3 (25D3) 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 1α-hydroxylase (CYP27B1), which converts inactive 25D3 to the active 1,25-dihydroxyvitamin D3 (1,25D3). Porcine rotavirus (PRV) infection alone resulted in a significant increase in CYP27B1 mRNA, which augmented the production of active vitamin D. Physiological concentrations of 25D3 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-β (IFN-β) promoter stimulator 1 (IPS-1) leading to the expression of type I interferons (IFN-β). Active 25D3 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-β and IFN-stimulated genes 15 (ISG15) with important innate immune functions. Inhibiting CYP27B1 also failed to increase RIG-I, IPS-1, IFN-β and ISG15 mRNA expression. These observations suggest that 25D3 can directly inhibit PRV in IPEC-J2 cells, which requires this active form of vitamin D. The anti-rotavirus effect of 25D3 is mediated at least in part by RIG-I signalling pathways in IPEC-J2 cells.
authors.affiliation: a College of Animal Science and Technology , Sichuan Agricultural University , Ya'an , P.R. China.
authors.forename: Ye
authors.initials: Y
authors.lastname: Zhao
authors.forename: Bing
authors.initials: B
authors.lastname: Yu
authors.forename: Xiangbing
authors.initials: X
authors.lastname: Mao
authors.forename: Jun
authors.initials: J
authors.lastname: He
authors.forename: Zhiqing
authors.initials: Z
authors.lastname: Huang
authors.forename: Ping
authors.initials: P
authors.lastname: Zheng
authors.forename: Jie
authors.initials: J
authors.lastname: Yu
authors.forename: Guoquan
authors.initials: G
authors.lastname: Han
authors.forename: Xiaofang
authors.initials: X
authors.lastname: Liang
authors.forename: Daiwen
authors.initials: D
authors.lastname: Chen
mesh_terms: D000818:Animals; D002112:Calcifediol / Q000494:pharmacology*; D002460:Cell Line / Q000187:drug effects; D004195:Disease Models, Animal; D015967:Gene Expression Regulation, Viral; D007413:Intestinal Mucosa / Q000821:virology*; D016133:Polymerase Chain Reaction / Q000662:veterinary; D012333:RNA, Messenger / Q000032:analysis; D018168:Receptors, Retinoic Acid / Q000235:genetics; D012401:Rotavirus / Q000235:genetics / Q000502:physiology*; D012400:Rotavirus Infections / Q000662:veterinary* / Q000821:virology; D013552:Swine; D013553:Swine Diseases / Q000821:virology*; D014779:Virus Replication
chemical_list: D012333:RNA, Messenger; D018168:Receptors, Retinoic Acid; D002112:Calcifediol
keywords: epithelium; gene expression; pigs; rotavirus; small intestine; vitamin D