hAD-MSCs Ameliorated Psoriasis-Like Skin Inflammation by Inhibiting the Neutrophil Migration.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background Psoriasis is a chronic inflammatory skin disease driven by an abnormal immune response. Mesenchymal stem cells have strong immunomodulatory properties. Therefore, we investigated the therapeutic effects and underlying mechanisms of human adipose-derived mesenchymal stem cells (hAD-MSCs) in a psoriasis-like mouse model. Methods A psoriasis-like mouse model was established and hAD-MSCs were administered via subcutaneous injection. Skin thickness was evaluated using hematoxylin and eosin (H&E) staining, and disease severity was assessed using the Psoriasis Area Severity Index (PASI). Neutrophil counts and Signal Transducer and Activator of Transcription 3 (STAT3) positive keratinocytes in the skin were evaluated by immunohistochemistry (IHC). Additionally, we evaluated the cytokine expression by quantitative PCR (q-PCR). Results hAD-MSCs significantly attenuated psoriasis-like skin inflammation. Neutrophil infiltration was markedly reduced in psoriatic lesions following hAD-MSC treatment. We found that hAD-MSCs inhibit neutrophil recruitment by lowering CXCL1 levels in the skin, which may be linked to reduced phosphorylation of STAT3. Conclusions Our findings highlight the potential of hAD-MSCs as a potent therapeutic strategy for inhibiting neutrophil recruitment and ameliorating psoriasis-like inflammation.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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