Abstract: Objective To investigate the effects of interleukin-33(IL-33)on HaCAT cells and psoriasis-like inflammation induced by imiquimod(IMQ) in mice. Methods Twenty-four hours after HaCAT cells were plated, the cell proliferation and autophagy-related protein were detect by CCK8 and Western blot. A psoriasis-like lesion model was established in mouse. Thirty female BALB/c mice of clean grade were randomly divided into three groups: control group, IMQ group, and IL-33 treatment group. After 6 days of continuous treatment, the lesions on the back of the mouse were observed. Results The treatment of IL-33 could enhance the proliferation of HaCAT cells and promote the expression of LC3, Beclin1 and p-STAT3 proteins. In the mouse psoriasis-like model, the thickened ear skin, scaly erythema and erythematous lesions on the back were seen and thickening of the epidermis, epidermal extension with parakeratosis were shown. These phenomena were more obvious in IL-33 treatment group(P＜0.05). The expression of autophagy-related proteins in the skin lesions of the IL-33 treatment group was significantly decreased compared with the control group and IMQ group(P＜0.05). Conclusions IL-33 promotes the proliferation of HaCAT cells, induces autophagy, and aggravates the occurrence and development of psoriatic lesions induced by imiquimod in mice, which may be involved in the activation of the STAT3 signaling pathway.

Key words: interleukin 33(IL-33), autophagy, STAT3, HaCAT cell