Abstract

The stratum corneum (SC) is such an efficient barrier that only 2-5 g per h per cm2 of transepidermal water loss (TEWL) occurs in normal skin. The SC also plays another important role at the skin surface in keeping our skin smooth and flexible by binding water. We exposed a simulation model of in vivo SC to various, excessive physical insults in vitro, such as irradiation with 1 J per cm2 of UVB, 50 J per cm2 of UVA, or 3000 rad of X-ray, heating at 90 degrees C for 3 min, freezing at -196 degrees C for 60 s or repeated placement in an extremely dry or humid condition. None of them could cause any permanent change in the SC functions. Only the application of chemical agents such as lipid solvents or a detergent or the affliction of trauma resulted in a functional derangement of the SC. Because the viable skin tissues are more vulnerable to the effects of the environment than the SC, most of the abnormalities of the SC functions developing after environmental insults are secondarily caused by enhanced epidermal proliferation induced under the influence of underlying inflammation. These functional abnormalities were found to be demonstrable with biophysical measurements long after the disappearance of skin redness, the clinically observable sign of inflammation. The SC abnormalities in inflamed skin are also detectable as a change in the content of chemical mediators. For example, the ratio between proinflammatory IL-1 and its receptor antagonist (IL-1ra) whose production by epidermal keratinocytes is markedly enhanced by various proinflammatory stimuli, showed a deviation towards an excess of the latter in inflammatory skin. Facial skin that is always exposed to the environment is unique in that its SC shows such a deviation in the IL-1/IL-1ra ratio suggestive for the presence of mild inflammation even in normal individuals.

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