Cutaneous barrier function after cold exposure in hairless mice: a model to demonstrate how cold interferes with barrier homeostasis among workers in the fish-processing industry.
Cutaneous barrier function after cold exposure in hairless mice: a model to demonstrate how cold interferes with barrier homeostasis among workers in the fish-processing industry.
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无毛小鼠寒冷暴露后的皮肤屏障功能：展示寒冷如何干扰鱼类加工业工人屏障稳态的模型。
DOI：
10.1111/j.1365-2133.1995.tb08672.x
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Feingold,KR
中科院分区：
文献类型：
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作者：
Halkier-Sørensen,L;Menon,GK;Elias,PM;Thestrup-Pedersen,K;Feingold,KR
丹麦鱼类加工业（FPI）的工人在工作期间很少发生皮肤干燥和湿疹，因为他们的手指和手掌皮肤表面温度低，经皮失水（TEWL）低，电容高。然而，工作后不久，当皮肤温度恢复正常时，TEWL水平上升到高于正常水平，电容下降到低于正常水平，随后出现皮肤干燥或皲裂，随后在数小时内恢复正常。这些观察结果表明，FPI工人的皮肤屏障功能可能存在缺陷，然而，这种缺陷被皮肤温度低所掩盖，从而导致工作期间TEWL水平低。为了验证这一假设，我们用局部丙酮破坏无毛小鼠的渗透性屏障，并将处理过的皮肤暴露在冰中3-5h。虽然在冷暴露后的TEWL率很低，表明屏障恢复正常，但当皮肤温度恢复正常（≥15min）时，TEWL增加到略高于冷暴露前的水平（即屏障被丙酮破坏后的水平）。TEWL的变化与电子密度示踪剂硝酸镧经皮渗透的等效变化是平行的。这表明寒冷掩盖了有缺陷的屏障，并抑制了屏障的修复。在环境温度下几个小时后，观察到正常的屏障恢复。在冷暴露后的前30分钟，电子显微镜显示空的或部分空的片层体。1 h后，大多数新生lb形态正常。此外，组织化学研究显示，冷暴露后角质层细胞间脂质的延迟再现。这些结果表明，冷暴露会阻止丙酮破坏后屏障的恢复，并为鱼类加工业和相关职业中观察到的职业性皮肤病提供了解释。
Dry skin and eczema only seldomly occur in workers in the Danish fish‐processing industry (FPI) during work, when their fingers and palms have a low skin surface temperature, low transepidermal water loss (TEWL), and a high capacitance. However, shortly after work, when the skin temperature has become normal, TEWL levels increase to above normal, and capacitance decreases to below normal, followed by the development of dry skin or chapping, which subsequently revert to normal over a period of hours. These observations suggest that workers in the FPI may have a delect in skin barrier function, which is, however, masked by a low skin temperature, resulting in misleadingly low TEWL levels during work. To test this hypothesis, we disrupted the permeability barrier in hairless mice with topical acetone, and exposed the treated skin to ice for 3–5h. Although TEWL rates immediately after cold exposure were low, suggesting normal barrier recovery, TEWL increased to levels slightly above pre‐cold exposure levels (i.e. levels just after the barrier was disrupted with acetone) when the skin temperature reverted to normal (≥ 15min). The changes in TEWL were paralleled by equivalent changes in percutaneous penetration of the electron‐dense tracer lanthanum nitrate. This indicates that cold masks a defective barrier, and inhibits barrierrepair. After a few hours at ambient temperatures, normal barrier recovery was observed. Electron microscopy revealed empty or partially empty lamellar bodies during the first 30 min post‐cold exposure. After 1 h the majority of nascent LBs displayed normal morphology. Moreover, histochemical studies showed a delayed reappearance of stratum corneum intercellular lipids following cold exposure. These results demonstrate that cold exposure prevents barrier recovery after acetone disruption, and provide an explanation for the occupatonal dermatosis observed in the fish‐processing industry and related occupations.