Study on the role and mechanism of P2X4 receptor in allergic contact dermatitis in mice

Allergic contact dermatitis (ACD) is a skin inflammation and immune disease, accompanied by persistent itching. These symptoms seriously affect the quality of life of patients. Trigeminal Ganglia (TG) play a key role in the facial sensory conduction and inflammatory regulation of ACD. It is reported that P2X4 receptor expressed in trigeminal ganglion neurons. Preliminary exploratory experiment showed the upregulated expression of P2X4 in TG during the pathophysiology of ACD. This study aims to investigate whether the P2X4 receptor in TG mediates the pathological changes of itching in ACD mouse models and its possible mechanisms. The results showed that the number of itchy and painful behaviors in ACD mice was increased, and the expression levels of P2X4 receptor, TRPA1 receptor, TNA-α, IL-1β and ROS in TG were significantly increased. In addition, the co-expression levels of NeuN with P2X4 and TRPA1 in TG neurons were increased, and the co-expression levels of P2X4 and PGP9.5 in the skin were increased, and all the above abnormal parameters were significantly reduced after treatment with P2X4 shRNA. The mechanism may be to decrease the expression and activity of TRPA1 receptor by reducing the secretion of inflammatory factors and the decrease of ROS production caused by the up-regulation of P2X4 receptor, reduce the influx of calcium ions, and improve the pathological changes of itching in ACD mouse models. P2X4 receptor may be a key target for the treatment of SADBE-induced ACD pathological changes.