Denda M, Sato J, Tsuchiya T, Elias P M, Feingold K R
Shiseido Research Center, Skin Biology Research Laboratories, Yokohama, Japan.
J Invest Dermatol. 1998 Nov;111(5):873-8. doi: 10.1046/j.1523-1747.1998.00364.x.
Although seasonal changes in humidity are thought to exacerbate various skin diseases, whether these flares can be attributed to prolonged exposure to extremes in environmental humidities has not been studied systematically. We recently showed that prolonged exposure to high versus low humidities induced profound changes in epidermal structure and permeability barrier homeostasis. Therefore, we asked here whether comparable extremes in humidity could initiate not only homeostatic, but also potentially pathophysiologic alterations. We showed first that exposure to low humidity increases epidermal DNA synthesis in normal murine epidermis. Moreover, exposure to a low humidity for 48 h further amplifies the DNA synthetic response to barrier disruption, resulting in marked epidermal hyperplasia. Additionally, exposure to a dry environment for 48 h prior to barrier disruption results in dermal mast cell hypertrophy, degranulation, as well as histologic evidence of inflammation. To demonstrate the role of changes in external moisture on these phenomena, we applied either an occlusive, water-impermeable plastic membrane, Petrolatum, or a nonocclusive humectant, both to nonperturbated and to perturbed skin. All three forms of treatment prevented the epidermal hyperplasia and dermal mast cell hypertrophy and degranulation induced by exposure to low humidity. These studies indicate that (i) exposure to changes in environmental humidity alone induces increased keratinocyte proliferation and markers of inflammation, and (ii) that these changes are attributable to changes in stratum corneum moisture content. Finally, these studies provide evidence that changes in environmental humidity contribute to the seasonal exacerbations/amelioration of cutaneous disorders, such as atopic dermatitis and psoriasis, diseases which are characterized by a defective barrier, epidermal hyperplasia, and inflammation.
尽管人们认为湿度的季节性变化会加剧各种皮肤疾病，但这些病情发作是否可归因于长期暴露于极端环境湿度尚未得到系统研究。我们最近发现，长期暴露于高湿度与低湿度环境会导致表皮结构和渗透屏障稳态发生深刻变化。因此，我们在此探讨，类似的极端湿度是否不仅会引发稳态变化，还可能引发病理生理改变。我们首先发现，暴露于低湿度环境会增加正常小鼠表皮中的DNA合成。此外，暴露于低湿度环境48小时会进一步放大对屏障破坏的DNA合成反应，导致明显的表皮增生。此外，在屏障破坏前暴露于干燥环境48小时会导致真皮肥大细胞肥大、脱颗粒，以及炎症的组织学证据。为了证明外部水分变化对这些现象的作用，我们对未受干扰和受干扰的皮肤都应用了封闭性、不透水的塑料膜、凡士林或非封闭性保湿剂。所有这三种治疗形式都能预防因暴露于低湿度环境而引起的表皮增生以及真皮肥大细胞肥大和脱颗粒。这些研究表明：（i）仅暴露于环境湿度变化就会导致角质形成细胞增殖增加和炎症标志物增加；（ii）这些变化可归因于角质层水分含量的变化。最后，这些研究提供了证据，证明环境湿度的变化会导致皮肤疾病（如特应性皮炎和银屑病）的季节性加重/缓解，这些疾病的特征是屏障缺陷、表皮增生和炎症。
