INTRODUCTION
The epidermis, the skin’s outermost layer, functions as a barrier against environmental aggressors through the cornification of keratinocytes to form the stratum corneum (SC). Embedded within a lipid matrix that mainly comprises cholesterol (CHOL), free fatty acids (FFAs), and ceramides (CERs), corneocytes undergo a maturation process that is essential to maintain proper SC barrier integrity and function.1
Solar ultraviolet radiation (UVR), comprised of ~95% UVA (320–400 nm) and ~5% UVB (280–320 nm), is a prominent environmental skin stressor.2 Numerous in vivo and ex vivo models have been developed to evaluate the impact of UVR on skin barrier, revealing mixed results. For instance, UVB and UVA irradiations were shown to increase SC triglycerides, FFAs, alkanes, and squalene levels in subjects with skin phototype II–III.3 Interestingly, UVB exposure alone decreases SC lipid cohesion and damages intercellular barrier permeability formed by tight-junctions.4,5 One research group evaluated the impact of UVR on skin biophysical properties on subjects with skin phototype II–IV. They found that UV exposure at various minimal erythema (MED) doses increased trans-epidermal water loss (TEWL) and decreased skin hydration in a dosedependent manner within 24 hours, suggesting impaired barrier function.6 Another study demonstrated that 1.5 MED did not affect skin hydration, but increased TEWL after 72 hours. They also observed a decrease in total CERs and increase in CHOL, indicating that alterations in SC lipid content in response to UV may disrupt barrier integrity.7
Under real life conditions, chronic sun-exposed hands of middleaged Japanese golfers were shown to be photodamaged and to have reduced skin hydration, but interestingly, no difference in TEWL compared to the glove-protected hands.8 It was also demonstrated in Chinese subjects that skin barrier recovery after tape-stripping was not as efficient for body sites exposed to sunlight compared to non-exposed.9 Overall, these findings indicate that depending on the nature of exposure and skin phototypes, UV-induced changes in skin barrier-related endpoints will greatly vary and may contradict one another. Thus, further studies are needed.
Prior studies have shown that application of an equal ratio of SC lipids promotes barrier repair, and increasing their ratios accelerate recovery.10 Because of their skin benefits, intercellular lipids, particularly CERs, are now commonly used as prominent ingredients in moisturizers for managing several dermatologic conditions.11–13 Moreover, many models have been used to evaluate the efficacy of various natural lipid mixtures for optimizing barrier repair in response to exogenous stimuli. For example, Byun et al reported that topical application of CHOL decreased elicited inflammatory response on tape-stripped human skin irradiated with UV while linoleic acid and N-oleoylphytosphingosine promoted cell death and inflammation, respectively.14 Additionally, synthetic CERs are also shown to promote faster barrier recovery after various stimuli, including UV and tape-stripping.15
Solar ultraviolet radiation (UVR), comprised of ~95% UVA (320–400 nm) and ~5% UVB (280–320 nm), is a prominent environmental skin stressor.2 Numerous in vivo and ex vivo models have been developed to evaluate the impact of UVR on skin barrier, revealing mixed results. For instance, UVB and UVA irradiations were shown to increase SC triglycerides, FFAs, alkanes, and squalene levels in subjects with skin phototype II–III.3 Interestingly, UVB exposure alone decreases SC lipid cohesion and damages intercellular barrier permeability formed by tight-junctions.4,5 One research group evaluated the impact of UVR on skin biophysical properties on subjects with skin phototype II–IV. They found that UV exposure at various minimal erythema (MED) doses increased trans-epidermal water loss (TEWL) and decreased skin hydration in a dosedependent manner within 24 hours, suggesting impaired barrier function.6 Another study demonstrated that 1.5 MED did not affect skin hydration, but increased TEWL after 72 hours. They also observed a decrease in total CERs and increase in CHOL, indicating that alterations in SC lipid content in response to UV may disrupt barrier integrity.7
Under real life conditions, chronic sun-exposed hands of middleaged Japanese golfers were shown to be photodamaged and to have reduced skin hydration, but interestingly, no difference in TEWL compared to the glove-protected hands.8 It was also demonstrated in Chinese subjects that skin barrier recovery after tape-stripping was not as efficient for body sites exposed to sunlight compared to non-exposed.9 Overall, these findings indicate that depending on the nature of exposure and skin phototypes, UV-induced changes in skin barrier-related endpoints will greatly vary and may contradict one another. Thus, further studies are needed.
Prior studies have shown that application of an equal ratio of SC lipids promotes barrier repair, and increasing their ratios accelerate recovery.10 Because of their skin benefits, intercellular lipids, particularly CERs, are now commonly used as prominent ingredients in moisturizers for managing several dermatologic conditions.11–13 Moreover, many models have been used to evaluate the efficacy of various natural lipid mixtures for optimizing barrier repair in response to exogenous stimuli. For example, Byun et al reported that topical application of CHOL decreased elicited inflammatory response on tape-stripped human skin irradiated with UV while linoleic acid and N-oleoylphytosphingosine promoted cell death and inflammation, respectively.14 Additionally, synthetic CERs are also shown to promote faster barrier recovery after various stimuli, including UV and tape-stripping.15
