Increased expression of IL‐33 in rosacea skin and UVB‐irradiated and LL‐37‐treated HaCaT cells

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Abstract
Background Rosacea is one of the most common dermatoses of adults. Although the detailed pathophysiology remains unknown, it is thought that rosacea is caused by a consistently aberrant, innate immune response, and that LL‐37 plays an important role. However, involvement of the inflammatory cytokine IL‐33 has not yet been studied. Objectives We explored the role played by IL‐33 in the pathophysiology of rosacea. Methods First, we immunohistochemically evaluated the expression of IL‐33 and its receptor (ST2) in rosacea skin. Second, we exposed HaCaT cells to ultraviolet B (UVB) irradiation in the presence or absence of LL‐37, and measured the expression of proinflammatory cytokines including IL‐33. We also analyzed VEGF (vascular endothelial growth factor) mRNA expression and protein release after co‐stimulation of HaCaT cells by LL‐37 and IL‐33. Results Immunohistochemically, IL‐33 expression was enhanced in the skin of rosacea patients, especially with erythematotelangiectatic subtype. In vitro, UVB and LL‐37 synergistically increased mRNAs expression of proinflammatory cytokines, especially IL‐33 and IL‐1β. IL‐33 protein release was also synergistically increased by LL‐37 and UVB treatment. LL‐37 and IL‐33 stimulated VEGF mRNA expression and VEGF release from HaCaT cells. Conclusions Our findings suggest that rosacea skin with abundant LL‐37 may robustly produce and release IL‐33 when exposed to UV radiation. IL‐33 may participate in the angiogenesis and vasodilation of rosacea skin by enhancing VEGF release.
Funding Information
  • National Research Foundation of Korea

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