Biomedical journal · 2025
Extracorporeal shockwave therapy ameliorates skin inflammation of imiquimod-induced psoriasis in mice.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Lin Shang-Hung, Cheng Po-Sheng, Hsiao Chang-Chun, Lee Chih-Hung
Аннотация
BACKGROUND: 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.
OBJECTIVE: 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.
MATERIAL AND METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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.
OBJECTIVE: 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.
MATERIAL AND METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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.