Department of Dermatology, Faculty of Medicine, Jichi Medical University, Tochigi 329-0498, Japan.
Int J Mol Sci. 2021 Apr 12;22(8):3970. doi: 10.3390/ijms22083970.
The production of melanin pigments by melanocytes and their quantity, quality, and distribution play a decisive role in determining human skin, eye, and hair color, and protect the skin from adverse effects of ultraviolet radiation (UVR) and oxidative stress from various environmental pollutants. Melanocytes reside in the basal layer of the interfollicular epidermis and are compensated by melanocyte stem cells in the follicular bulge area. Various stimuli such as eczema, microbial infection, ultraviolet light exposure, mechanical injury, and aging provoke skin inflammation. These acute or chronic inflammatory responses cause inflammatory cytokine production from epidermal keratinocytes as well as dermal fibroblasts and other cells, which in turn stimulate melanocytes, often resulting in skin pigmentation. It is confirmed by some recent studies that several interleukins (ILs) and other inflammatory mediators modulate the proliferation and differentiation of human epidermal melanocytes and also promote or inhibit expression of melanogenesis-related gene expression directly or indirectly, thereby participating in regulation of skin pigmentation. Understanding of mechanisms of skin pigmentation due to inflammation helps to elucidate the relationship between inflammation and skin pigmentation regulation and can guide development of new therapeutic pathways for treating pigmented dermatosis. This review covers the mechanistic aspects of skin pigmentation caused by inflammation.
黑素细胞产生的黑色素及其数量、质量和分布在决定人类皮肤、眼睛和头发颜色方面起着决定性作用，并保护皮肤免受紫外线辐射 (UVR) 和各种环境污染物的氧化应激的不利影响。黑素细胞位于毛囊间表皮的基底层，由毛囊隆起区域的黑素细胞干细胞补偿。湿疹、微生物感染、紫外线照射、机械损伤和衰老等各种刺激会引发皮肤炎症。这些急性或慢性炎症反应会导致表皮角质形成细胞以及真皮成纤维细胞和其他细胞产生炎性细胞因子，进而刺激黑素细胞，通常导致皮肤色素沉着。一些最近的研究证实，几种白细胞介素 (IL) 和其他炎症介质调节人表皮黑素细胞的增殖和分化，并直接或间接促进或抑制黑色素生成相关基因表达，从而参与皮肤色素沉着的调节。对炎症引起的皮肤色素沉着机制的理解有助于阐明炎症与皮肤色素沉着调节之间的关系，并为治疗色素性皮肤病的新治疗途径的发展提供指导。这篇综述涵盖了炎症引起的皮肤色素沉着的机制方面。
