C3AR1 regulates intestinal T-cell immune response after burn by activating the NF-κB signaling pathway.

Abstract

Severe burns are characterized by high mortality and morbidity rates. Immune dysfunction during the acute phase of severe burns exacerbates tissue damage. Complement C3a receptor 1 (C3AR1) is a key receptor associated with severe burn shock. This study aimed to investigate the effects of C3AR1 on T-cell immunity in the intestine following burns. We established a mouse model of severe burns and performed in vitro stimulation of CD3T cells with C3AR1 agonist. Quantitative real-time PCR, Western blot, ELISA, and flow cytometry were used to analyze the expression of C3AR1, IL-2, IL-10 and factors related to the NF-κB signaling pathway, changes in the proportions of Th1 and Th2 subsets, and the apoptosis rate of CD3T cells after C3AR1 stimulation. The results showed that C3AR1 expression in the intestinal mucosa of severely burned mice was significantly elevated, while IL-2 expression was decreased, exhibiting a negative correlation. After C3AR1 overexpression, the proportion of Th1 cells decreased, the apoptosis rates of Th2 cells and CD3T cells increased, IL-2 expression was reduced, and the NF-κB signaling pathway was activated. In conclusion, C3AR1 participates in intestinal T-cell immune responses after burns through activation of the NF-κB signaling pathway, indicating that C3AR1 is a crucial regulator in the recovery of intestinal mucosal injury and immune function balance, and may serve as a potential molecular target for burn treatment.