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.