Abstract
The present study investigated the role of colchicine in the treatment of RSV infection. Treatment of BEAS-2B cells following RSV infection with colchicine caused a significant decrease in the number of viral plaques. In RSV-infected BEAS-2B cells' treatment with colchicine leads to a significant up-regulation of both IFN-β1 and RIG-I genes. The levels of interleukin, NO, and MDA were suppressed in BEAS-2B cells infected with RSV by colchicine. The phosphorylation of Stat3, COX-2, and p38 was also suppressed significantly by colchicine. The phosphorylation of IkBα was promoted in RSV-infected BEAS-2B cells' oncolchicine treatment. In neonatal rats, replication of RSV was inhibited significantly by colchicine treatment which was evident by suppression of RSV-L gene expression. A significant decrease in the level of IL-6 and TNF-α was caused in neonatal rat BALF by colchicine treatment. The production of MDA, NO and MPO in the neonatal rat BALF was suppressed markedly by colchicine treatment. Treatment of the neonatal rats infected by RSV with colchicine suppressed the release of IκBα and COX-2 in the pulmonary epithelial cells. Colchicine treatment of the neonatal rats promoted the expression of IFN-α and IFN-β1. In summary, the current study showed that colchicine inhibited RSV infection in neonatal rats through regulation of anti-oxidative factor production. The expression of IFN-β1 and RIG-I genes was also up-regulated in the RSV-infected alveolar epithelial cells by treatment with colchicine. Therefore, colchicine may be developed as the therapeutic agent for the treatment of RSV infection.