Increased expression of IL-33 in rosacea skin and UVB-irradiated and LL-37-treated HaCaT cells
- 주제(키워드) cathelicidin , IL-33 , LL-37 , rosacea , ultraviolet B , vascular endothelial growth factor
- 주제(기타) Dermatology
- 설명문(일반) [Suhng, Eunah] Yonsei Gowoon Dermatol Clin, Seoul, South Korea; [Choi, You Won; Choi, Hae Young; Byun, Ji Yeon] Ewha Womans Univ, Dept Dermatol, Coll Med, Seoul, South Korea; [Kim, Bo Hee; Cho, Hyunjin] Dongguk Univ, Res Inst Integrat Regenerat Biomed Engn, Seoul, South Korea
- 등재 SCIE, SCOPUS
- 발행기관 WILEY
- 발행년도 2018
- URI http://www.dcollection.net/handler/ewha/000000155765
- 본문언어 영어
- Published As http://dx.doi.org/10.1111/exd.13702
초록/요약
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. We explored the role played by IL-33 in the pathophysiology of rosacea. 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 analysed VEGF (vascular endothelial growth factor) mRNA expression and protein release after costimulation of HaCaT cells by LL-37 and IL-33. 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-1. 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. 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.
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