Extracorporeal shockwave therapy ameliorates skin inflammation of imiquimod-induced psoriasis in mice

Psoriasis is a chronic inflammatory disease characterized by abnormal keratinocyte proliferation and dermal inflammation. TNF-α and IL-17/23 play significant roles in the pathophysiology of psoriasis. The immunomodulatory effect of extracorporeal shockwave therapy (ESWT) has been widely applied in the treatment of chronic inflammatory disorders.

This study aimed to investigate the effect of ESWT on imiquimod (IMQ)-induced psoriatic lesions and the mechanisms by which ESWT affects macrophages and T cell subsets.

Five groups of mouse models were included: wild type (WT) mice without treatment, mice receiving ESWT alone, mice treated with IMQ alone, mice treated with IMQ and ESWT (n = 6), and mice treated with IMQ and adalimumab (anti- TNF-α). We measured epidermal thickness, inflammatory cell infiltration, and the levels of inflammatory cytokines in the skin.

The increase in epidermal thickness caused by IMQ was substantially reduced by ESWT or adalimumab. In parallel, the increased number of IL17⁺ cells, along with the increased IL-23 and TNF-α induced by IMQ, decreased significantly after ESWT or adalimumab treatment. However, the IMQ-induced increase in the number of M1 and M2 macrophages was reduced selectively by ESWT, but not by adalimumab. Moreover, in vitro experiments revealed that ESWT decreased TNF-α production by M1 macrophages but increased IL-10 production by M2 macrophages.

ESWT significantly reduced epidermal thickness, macrophage and IL-17⁺ cell infiltration, and the expression of IL-23 and TNF-α in IMQ-induced psoriasis mice. These findings suggest that ESWT may ameliorate psoriatic skin lesions by modulating macrophage activity and IL-17⁺ cell-mediated inflammation.