TLR2 affects CD86 expression and inflammatory response in burn injury mice through regulation of p38.

Abstract

The aim of this study was to assess the effects of TLR2-p38-CD86 signaling pathways on the inflammatory response in a mouse model of burn injury. Wild-type (TLR2+/+) and mutant-type (TLR2-/-) mice were obtained, and a mouse burn injury model was constructed. Tissue samples were examined with hematoxylin and eosin staining and the transferase mediated nick end labeling (TUNEL) method. Macrophages were treated with TLR2 agonist and p38 inhibitor. The expression levels of TLR2, p38, CD86, IL-1β, and TNF-α were quantified by RT-qPCR, Western blot, and ELISA. When compared with the sham group, the burn group had a significantly higher rate of apoptosis as well as higher expressions of TLR2, p38, CD86, IL-1β, and TNF-α. Inhibiting TLR2 was shown to significantly reduce the expressions of p-p38, CD86, IL-1β, and TNF-α. In the results of in-vitro experiments, TLR2 agonist increased the expression of p-p38, CD86, IL-1β, and TNF-α, whereas a p38 inhibitor was shown to reduce the expression of CD86, IL-1β, and TNF-α. Our results suggest that the TLR2-p38-CD86 signaling pathway plays a vital role in inflammation associated with burn injury.