Objectives: Chikungunya virus (ChikV) infection is characterized by persistent infection in joints and lymphoid organs. The ChikV Capsid protein plays an important role in regulating virus replication. In this study, we hypothesized that capsid protein may stimulate dendritic cell (DC) activation and maturation and trigger an inflammatory response in mice.
Materials and methods: Mice were intraperitoneally injected with capsid protein and examined for changes in immunophenotype in lymph nodes (LNs). Next, DCs were treated with capsid protein or LPS and then expression of maturation markers, cytokine production, and ability to stimulate CD4+ T cells in allo-MLR were analyzed.
Results: Injection of mice with capsid protein led to recruitment of myeloid cells and increased activation of T lymphocytes in LNs. Importantly, treatment of DCs with capsid protein prolonged the activation of IKB-α and up-regulated the number of CD11c+CD86+DCs and release of TNF-α and IL-12p70 as well as reducing DC apoptosis, all effects were abolished in the presence of Bay 11-7082. In addition, IL-2 production was higher by CD4+ T cells stimulated with capsid-treated as compared with LPS-induced DCs.
Conclusion: The observations revealed that capsid protein participates in the regulation of NF-κB signaling and maturation of DCs.
Keywords: Chikungunya virus; Cytokine; Dendritic cell; MAPK; NF-κB.