Murine bone marrow-derived DCs activated by porcine rotavirus stimulate the Th1 subtype response in vitro

•Evidence is accumulating that rotavirus affects intestinal epithelial cells and triggers innate immune responses.•However, little is known about the mucosal immune response after PRV infection.•We studied the interaction of bone marrow-derived DCs (BMDCs) from BALB/c mice with the DN30209 strain of PRV and their interaction mechanism in vitro.•We identified the mechanisms that DCs use to modulate the mucosal immune response, and Toll-like receptor (TLR) signaling pathways play a major role in PRV-stimulated BMDCs.•The results demonstrated that the activation of BMDCs occurred in both MyD88-independent (TLR3) and MyD88-dependent (TLR2) pathways to initiate the NF-κB activation, the PRV-stimulated BMDCs preferentially promoted a Th1-type T cell response.

Rotavirus (RV) infection causes acute, watery dehydrating diarrhea and even death in infants and other young animals, resulting in a severe economic burden; however, little is known about the innate immune mechanisms associated with RV infection. Dendritic cells (DCs), which are professional antigen-presenting cells (APCs), serve as a bridge connecting the innate and adaptive immune system. In this study, the interaction between murine bone marrow-derived DCs (BMDCs) and porcine rotavirus (PRV) was investigated in vitro. Upon stimulation, the expression levels of MHC-II, CD40, CD80, CD86 and CD83 in BMDCs increased in a time-dependent manner, indicating activation and maturation by PRV. In addition, up-regulated Toll-like receptor 2 (TLR2), TLR3 and NF-κB increased the production of interleukin-12 and interferon-γ. The PRV-stimulated BMDCs also showed increased stimulatory capacity in mixed lymphocyte reactions and promoted the Th1 subtype response.