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

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 CD3⁺ T 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 CD3⁺ T 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 CD3⁺ T 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.