| Summary: | The mechanism of action of IPL in acne treatment is not clearly understood, but an immunomodulatory role has been suggested. Furthermore, inflammatory cytokines and matrix degrading enzymes play a key role in acne pathogenesis. Therefore, curbing the production of these mediators may assist acne resolution. In photorejuvenation studies, IPL has been shown to induce the expression of a key immunomodulatory cytokine, TGF-β. Interestingly, TGF-β has been demonstrated to mediate immunosuppression, inhibition of keratinocyte proliferation and MMP-1 repression through a Smad3-mediated signalling pathway. Therefore, we sought to investigate the in vivo effects of IPL used for acne treatment. Biopsies obtained from 20 patients with inflammatory acne vulgaris at baseline and post-IPL treatment (48 hrs after the first treatment and 1 week after the final treatment) were immunohistochemically analysed to investigate the expression of TGF-β1, TGF-β2, TGF-β3, Smad3, MMP-1 and IL-8. Digital images were semi-qualitatively assessed using image analysis software. In addition, quantitative PCR analysis of TGF-β1, Smad3 and IL-8 was performed on biopsies from seven cases. Immunohistochemical analysis demonstrated that IPL elicited a statistically significant increase in epidermal TGF-β1 expression. However, no statistically significant difference was observed in the expression of TGF-β2/β3. Increased nuclear immunolocalisation of Smad3 was demonstrated in the post-IPL biopsies, which was statistically significant. Although not statistically significant, both IL-8 and MMP-1 expression showed a downward trend in the majority of cases. No statistically significant change was detected in the gene expression of TGF-β1, Smad3 and IL-8, which may be attributed to the small sample in which PCR was carried out. The data from this study suggests that Smad3-mediated TGF-β1 signalling may play a role in IPL-induced resolution of acne vulgaris. The therapeutic effect of TGF-β1 in inflammatory acne vulgaris could be attributed to its immunosuppressive effect and its ability to inhibit matrix degradation and keratinocyte proliferation.
|
|---|
