Botulinum Toxin A Modulates Keratinocyte Proliferation and Inflammatory and Pruritic Mediators in Wound Healing
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Background: Botulinum toxin type A (BTA) is widely used in dermatologic procedures. While its anti-fibrotic effects on fibroblasts are well established, its role in keratinocyte-driven inflam- mation and pruritus during wound healing remains underexplored. Objective: To evaluate the effects of BTA on keratinocyte proliferation, migration, and trans- forming growth factor-beta (TGF-β)—induced expression of inflammatory and pruritus-asso- ciated mediator. Methods: Human epidermal keratinocytes were stimulated with TGF-β to mimic wound condi- tions, followed by BTA co-treatment. Cell proliferation and migration were assessed using water soluble tetrazolium salt-8 and scratch assays. Western blotting evaluated Smad2/3 and extracel- lular signal-regulated kinase (ERK)1/2 phosphorylation. Reverse transcription-quantitative poly- merase chain reaction was used to quantify inflammatory cytokines and itch-related mediators. Results: BTA significantly enhanced keratinocyte proliferation without affecting migration. It inhibited TGF-β–induced phosphorylation of Smad2/3 and ERK1/2. BTA also downregulated pro-inflammatory cytokines (interleukin [IL]-1β, IL-6, tumor necrosis factor-α, monocyte chemotactic protein 1, prostaglandin E synthase) and pruritus-related mediators (IL-31, IL-33, cathepsin S, calcitonin gene-related peptide, substance P, and thymic stromal lymphopoietin). Conclusion: BTA promotes keratinocyte proliferation and reduces TGF-β–induced inflamma- tory and pruritus-associated mediators. These findings suggest that BTA may facilitate wound healing by promoting keratinocyte proliferation while simultaneously modulating inflamma- tion and pruritic responses.
Abstract
Background: Botulinum toxin type A (BTA) is widely used in dermatologic procedures. While its anti-fibrotic effects on fibroblasts are well established, its role in keratinocyte-driven inflam- mation and pruritus during wound healing remains underexplored. Objective: To evaluate the effects of BTA on keratinocyte proliferation, migration, and trans- forming growth factor-beta (TGF-β)—induced expression of inflammatory and pruritus-asso- ciated mediator. Methods: Human epidermal keratinocytes were stimulated with TGF-β to mimic wound condi- tions, followed by BTA co-treatment. Cell proliferation and migration were assessed using water soluble tetrazolium salt-8 and scratch assays. Western blotting evaluated Smad2/3 and extracel- lular signal-regulated kinase (ERK)1/2 phosphorylation. Reverse transcription-quantitative poly- merase chain reaction was used to quantify inflammatory cytokines and itch-related mediators. Results: BTA significantly enhanced keratinocyte proliferation without affecting migration. It inhibited TGF-β–induced phosphorylation of Smad2/3 and ERK1/2. BTA also downregulated pro-inflammatory cytokines (interleukin [IL]-1β, IL-6, tumor necrosis factor-α, monocyte chemotactic protein 1, prostaglandin E synthase) and pruritus-related mediators (IL-31, IL-33, cathepsin S, calcitonin gene-related peptide, substance P, and thymic stromal lymphopoietin). Conclusion: BTA promotes keratinocyte proliferation and reduces TGF-β–induced inflamma- tory and pruritus-associated mediators. These findings suggest that BTA may facilitate wound healing by promoting keratinocyte proliferation while simultaneously modulating inflamma- tion and pruritic responses.