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首页> 外文期刊>Journal of dermatological science >Regulatory roles of sex hormones in cutaneous biology and immunology.
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Regulatory roles of sex hormones in cutaneous biology and immunology.

机译：性激素在皮肤生物学和免疫学中的调节作用。

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摘要

Recent studies have revealed that sex hormones manifest a variety of biological and immunological effects in the skin. Pregnancy, menstruation and the menopause modulate the natural course of psoriasis, indicating a female hormone-induced regulation of skin inflammation. Estrogen in vitro down-regulates the production of the neutrophil, type 1 T cell and macrophage-attracting chemokines, CXCL8, CXCL10, CCL5, by keratinocytes, and suppresses IL-12 production and antigen-presenting capacity while enhancing anti-inflammatory IL-10 production by dendritic cells. These data indicate that estrogen may attenuate inflammation in psoriatic lesions. Estrogen, alone or together with progesterone, prevents or reverses skin atrophy, dryness and wrinkles associated with chronological or photo-aging. Estrogen and progesterone stimulate proliferation of keratinocytes while estrogen suppresses apoptosis and thus prevents epidermal atrophy. Estrogen also enhances collagen synthesis, and estrogen and progesterone suppress collagenolysis by reducing matrix metalloproteinase activity in fibroblasts, thereby maintaining skin thickness. Estrogen maintains skin moisture by increasing acid mucopolysaccharide or hyaluronic acid levels in the dermis. Progesterone increases sebum secretion. Estrogen accelerates cutaneous wound healing stimulating NGF production in macrophages, GM-CSF production in keratinocytes and bFGF and TGF-beta1 production in fibroblasts, leading to the enhancement of wound re-innervation, re-epithelialization and granulation tissue formation. In contrast, androgens prolong inflammation, reduce deposition of extracellular matrix in wounds, and reduce the rate of wound healing. Estrogen enhances VEGF production in macrophages, an effect that is antagonized by androgens and which may be related to the development of granuloma pyogenicum during pregnancy. These regulatory effects of sex steroids may be manipulated as therapeutic or prophylactic measures in psoriasis, aging, chronic wounds or granuloma pyogenicum.
机译：最近的研究表明，性激素在皮肤中表现出多种生物学和免疫学作用。怀孕，月经和更年期会调节牛皮癣的自然进程，表明女性荷尔蒙引起的皮肤炎症调节。体外雌激素通过角质形成细胞下调中性粒细胞，1型T细胞和吸引巨噬细胞的趋化因子CXCL8，CXCL10，CCL5的产生，并抑制IL-12产生和抗原呈递能力，同时增强抗炎性IL-10树突状细胞的产生。这些数据表明，雌激素可以减轻牛皮癣病变中的炎症。雌激素单独或与孕激素一起使用，可预防或逆转与时间顺序或光老化相关的皮肤萎缩，干燥和皱纹。雌激素和孕激素刺激角质形成细胞的增殖，而雌激素则抑制细胞凋亡，从而防止表皮萎缩。雌激素还增强胶原蛋白的合成，雌激素和孕酮通过减少成纤维细胞中的基质金属蛋白酶活性来抑制胶原蛋白分解，从而保持皮肤厚度。雌激素通过增加真皮中酸性粘多糖或透明质酸的含量来维持皮肤水分。孕酮增加皮脂分泌。雌激素可加速皮肤伤口愈合，从而刺激巨噬细胞中NGF的产生，角质形成细胞中GM-CSF的产生以及成纤维细胞中bFGF和TGF-β1的产生，从而导致伤口重新神经支配，重新上皮化和肉芽组织形成。相反，雄激素延长炎症，减少伤口中细胞外基质的沉积，并降低伤口愈合的速度。雌激素可增强巨噬细胞中VEGF的产生，这种作用被雄激素拮抗，可能与妊娠期化脓性肉芽肿的发展有关。性类固醇的这些调节作用可作为牛皮癣，衰老，慢性伤口或化脓性肉芽肿中的治疗或预防措施进行操纵。

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