Induction of IFN- β through both TLR-3- and RIG-I-mediated signaling pathways in canine respiratory epithelial cells infected with H3N2 canine influenza virus

In this study, we aimed to determine the signaling pathways leading to the induction of IFN-β in a canine respiratory epithelial cell line (i.e., KU-CBE) infected with the H3N2 subtype of CIV. Small interfering RNAs (siRNAs) specific to pattern recognition receptors (PRRs) and transcription factors were used to block the IFN-β-induction signals in H3N2 CIV-infected KU-CBE cells. Among the PRRs, only the TLR3 and RIG-I expression levels significantly (P < 0.001) increased in CIV-infected cells. Following transfection with siRNA specific to TLR3 (siTLR3) or RIG-I (siRIG-I), the mRNA expression levels of IFN-β significantly (P < 0.001) decreased, and the protein expression of IFN-β also decreased in infected cells. In addition, co-transfection with both siTLR3 and siRIG-I resulted in the significant reduction of IRF3 (P < 0.001) and IFN-β (P < 0.001) mRNA levels. Moreover, the protein concentration of IFN-β was significantly (P < 0.01) lower in cells co-transfected with both siTLR3 and siRIG-I than in cells transfected with either siTLR3 or siRIG-I alone. The antiviral protein MX1was only expressed in KU-CBE cells infected with CIV or treated with IFN-β or IFN-α. Thus, we speculate that the IFN-β further induces MX1 expression that might suppress CIV replication. These data indicate that TLR3 and RIG-I synergistically induce IFN-β expression via the activation of IRF3. The IFN-β produced further induces the production of MX1, which would suppress CIV re...
Source: Journal of Microbiology and Biotechnology - Category: Biotechnology Authors: Source Type: research