Search

Background Dry skin in atopic dermatitis (AD) mainly results from barrier impairment due to deficiency of ceramide and natural moisturizing factors including pyrrolidone carboxylic acid (PCA) in stratum corneum (SC). Caspase-14 cleaves filaggrin monomers to free amino acids and their derivatives such as PCA, contributing natural moisturizing factors. Cytokines in the corneocytes represent cutaneous inflammation severity of AD patients. Object To analyze the correlations of PCA, caspase-14 and cytokines in corneocytes with clinical severity, barrier function and skin inflammation, those were quantitated. Methods A total of 73 persons were enrolled: 21 patients with mild AD, 21 with moderate-to-severe AD, 13 with X-linked ichthyosis (XLI) as a negative control for filaggrin gene (FLG) mutation, and 18 healthy controls. Skin barrier functions such as basal transepidermal water loss (TEWL), stratum corneum (SC) hydration and skin surface pH were measured. To collect corneocytes, stripping with D-squame® discs was done on lesional and non-lesional skin. And then PCA was isolated from D-squame® discs and quantitated by LC–MS/MS. Cytokine assays were performed. Results The quantity of PCA and caspase-14 was decreased in inflammatory lesions compared to non-lesion in AD patients. And the amounts of PCA and caspase-14 in the lesion of AD patients correlated with clinical severity as determined by eczema area and severity index score and the skin barrier functions. Also, the expressions of TNF-α and IL-13 inversely correlated with PCA quantity. Conclusion The quantity of PCA or caspase-14 in the corneocytes of the lesional skin of AD patients reflects the clinical severity, skin barrier function and the degree of lesional inflammation.

Background Atopic dermatitis (AD) shows dry skin. Water-soluble, low molecular weight components, collectively known as natural moisturizing factor (NMF), play an important role in maintaining the stratum corneum (SC) hydration. Previous studies focused on reduced levels of free amino acids (FAAs) in NMF from AD skin. It remains unknown, however, whether other NMF components are also altered in AD. Objective To characterize the levels of various NMF components in the SC of healthy subjects and in mild AD adult patients. Methods NMF components were extracted from three sequential tape-stripped SC samples obtained from the volar forearm. NMF components which were decreased in AD skin were topically applied to examine their contribution to SC moisturization in AD skin. Results We found that although FAAs levels were not remarkably reduced, levels of pyrrolidone carboxylic acid (PCA), lactate, urea, sodium and potassium were significantly decreased in NMF from mild AD skin. Among those components, only the topical application of potassium lactate effectively increased skin surface hydration indicating that reductions of lactate and potassium influence dry skin in mild AD patients. Unlike the distribution of filaggrin-derived FAAs and PCA, lactate, urea, potassium and sodium were abundant in the surface layer of the SC compared with the inner layer of the SC. Such findings strongly suggest that those components are supplied from outside the SC, i.e. they originate from sweat. Conclusion The reduced levels of sweat-derived NMF components in mild AD patients suggests that impaired sweat function might in part result in the SC dryness.

Background Dry skin causes pruritus and discomfort in patients with xerosis and atopic dermatitis. General treatment for skin dryness involves the topical application of an emollient. However, more effective, simpler therapies are desired. Collagen tripeptide (CTP) is a highly purified, non-antigenic, low-allergenic collagen fraction that is known to have various biological effects. Objective To clarify the therapeutic effects of CTP for dry skin using acetone-induced dry skin model mice. Methods ICR mice were treated with acetone followed by oral administration of CTP (80 or 500 mg/kg/day) for 3 days. Hyaluronic acid production induced by CTP was assessed using human dermal fibroblasts in vitro and in an acetone-induced dry skin model mice in vivo. Transepidermal water loss (TEWL) and scratching behavior were evaluated. Furthermore, the effects of CTP on intraepidermal nerve fibers and expression of semaphorin 3A (Sema3A) and nerve growth factor (NGF) were examined by immunohistochemistry and quantitative RT-PCR. Results CTP enhanced hyaluronic acid production in human dermal fibroblasts in vitro and in murine skin in vivo. Oral administration of CTP in acetone-induced dry skin model mice significantly decreased TEWL and suppressed scratching behavior. Intraepidermal nerve growth was dramatically inhibited in CTP-treated mice. Quantitative PCR analysis and immunohistochemical study revealed that CTP abolished the increased NGF and decreased Sema3A levels induced by acetone treatment. Conclusion Oral administration of CTP improves dry skin and normalizes axon-guidance factors in the epidermis in addition to reducing pruritus. CTP may be used in a new therapeutic strategy against dry skin and pruritus.

Background Glycosaminoglycans (GAGs) have various structural and physiological regulatory functions in skin, including tissue water maintenance, due to their high water-holding capacity. Objective To investigate changes of GAGs during intrinsic aging and photoaging of human skin and their correlations with water content. Methods Samples of sun-protected buttock and sun-exposed forearm skin were obtained from young male (21–30years, n =8) and female (20–33years, n =8) subjects, as well as old male (70–78years, n =8) and female (70–80years, n =8) subjects, and their epidermal and dermal contents of hyaluronic acid (HA), total sulfated GAG (tsGAG), total uronic acid (tUA), and tissue water were measured. HA content was determined by enzyme-linked immunosorbent assay using HA-binding protein, tsGAG by the sulfated GAG assay kit using 1,9-dimethylmethylene blue, tUA by carbazole reaction, and tissue water by subtraction of tissue dry weight from wet weight. Results In the buttock, HA was higher in dermis than in epidermis, while tsGAG and tUA were higher in epidermis. In intrinsically aged buttock, epidermal HA and dermal tsGAG and tUA decreased. However, when analyzed for each gender, epidermal tsGAG, tUA, and tissue water decreased only in females. Forearm/buttock ratios of each molecule were compared for determination of photoaging-dependent changes. Forearm/buttock ratios of HA, tsGAG, tUA, and tissue water increased in aged dermis, but showed no change in aged epidermis. When analyzed for each gender, ratios of epidermal HA and tissue water increased only in aged females, while ratios of epidermal tsGAG, tUA, and tissue water decreased only in aged males. Correlations of water content with HA, tsGAG, and tUA were found in epidermis, but not with tsGAG in dermis. Conclusion These intrinsic aging- and photoaging-dependent GAG changes and their correlations with water content provide new insights into the pathophysiology of dry skin in the elderly.

Summary Background Skin dryness is apparent in several pruritic skin diseases, such as xerosis and atopic dermatitis. Our previous study has demonstrated an increase of nerve fibers in the epidermis of patients with xerosis, suggesting the contribution of nerve fibers to itching. Objective This study was conducted to reveal a direct linkage between dry skin and intraepidermal nerve growth. Methods ICR mice treated with acetone were used as a dry skin model. Time-dependent measurement of transepidermal water loss (TEWL) and stratum corneum (SC) hydration was performed on the treated areas. Moreover, both the distribution of intraepidermal nerve fibers and the expression of epidermal nerve growth factor (NGF) and amphiregulin (AR) were examined sequentially with immunohistochemistry and quantitative RT-PCR. The same experiments were carried out in control mice treated with sterile water. Results Enhanced TEWL and decreased SC hydration were observed in the acetone-treated skins during the first hour after the treatment. These parameters gradually returned to the normal range within 48 h. In the acetone-treated mice, we found that there were many nerve fibers in the epidermis between 16 and 48 h after the treatment. No changes of the parameters for barrier disruption and intraepidermal nerve growth were observed in the control skins. Moreover, the expression of epidermal NGF and AR at the protein and mRNA levels was increased before the penetration of nerve fibers into the epidermis. Conclusions These results suggest that increases of epidermal NGF and AR levels are associated with intraepidermal nerve growth in acetone-treated mice.

Background Pruritus and discomfort are often present in patients with xerosis and atopic dermatitis. Several studies suggest an important role of diet in skin pathophysiology. Objective This study evaluated the effect of dietary fatty acids in the skin physiology via an itch-related animal model with and without supplementation with fish oil (FO), a source of polyunsaturated fatty acids (PUFA), especially omega 3 ( n -3). Methods Male Wistar rats were divided into two groups—non-supplemented (control) and supplemented with FO (3 g/kg/day) by gavage for 90 days. Every 30 days, scratching and skin parameters (transepidermal water loss (TEWL), hydration, and local blood flow) were evaluated before and after dorsal skin exposure to acetone to induce the itch-related dry skin. At the end of the study, animals were sacrificed, and skin samples collected for fatty acids composition analysis by GC–FID. Results FO supplementation reduced the TEWL and increased the skin hydration, with significant changes from day 60 on, while skin microcirculation registered no changes. It also alleviated the acetone induced skin barrier alteration, revealed by a faster resolution of TEWL and hydration, and elimination of itch-related scratching induced by dry skin. These changes were associated with the shift in the skin fatty acids incorporation pattern (richer in n -3 with n -6/ n -3 Conclusion Skin barrier dynamics seem to be influenced by FO n -3 PUFA, with suppressive effects on the scratching behaviour induced by dry skin. Hence, long-term supplementation with n -3 PUFA rich nutrients might reinforce and restore cutaneous integrity and function.

Summary Background: It is recognized that colonization by Staphylococcus aureus (SA) on the skin is one of the factors that can worsen atopic dermatitis (AD). Antibiotics and germicides are not the best choice to remove bacteria from the skin of AD patients, because of problems of irritation to the skin and bacterial resistance. We therefore turned our attention to the biofilm of SA with the aim of removing only SA from the skin surface of AD patients. We found that xylitol (X) and farnesol (F) synergistically inhibited biofilm formation by SA and dissolved biofilm formed in vivo (Part 1). Objective: To test whether application of AD for 1 week with FX cream can reduce SA without affecting Staphylococcus epidermidis. Methods: A randomized, double-blind, placebo-controlled right-and-left comparison study was performed. The arms of 17 patients with dry-type AD were applied with skin-care cream including/or not including a 0.02% F and 5% X combination for 1 week. The clinical response, biophysical assessment of the skin surface and counts of skin microflora were recorded before and after 1 week of therapy. Results: The ratio of SA in total bacteria at sites to which FX cream had been applied was significantly decreased after 1 week (P = 0.007), compared with before application and with placebo sites (P = 0.045). The mean skin conductance (a parameter indicating the state of hydration of the skin surface) of FX cream sites was increased significantly compared with the conductance before application (P = 0.0001) and at placebo sites (P = 0.002). Conclusion: This study provides evidence supporting the idea that cream containing F and X is a useful skin-care agent for atopic dry skin colonized by SA.

Summary Background: Staphylococcus aureus (SA) is usually present in atopic dry skin, and not only in regions seriously affected by atopic dermatitis. SA discharges various toxins and enzymes that injure the skin, and forms a biofilm from fibrin fiber and glycocalyx; the biofilm is important for adhesion of SA to the skin and for resistance to anti-microbial agents. Even highly effective moisturizers do not work perfectly on atopic dry skin. Staphylococcus epidermidis (SE) is a major constituent of skin microflora on healthy human skin, and provides protection against the growth of pathogenic bacteria. Objectives: Since treatment with anti-microbials may lead to re-growth of SA, which grows faster than other Staphylococci and often shows antibiotic resistance, we searched for novel approaches to control the skin-microfloral balance without using conventional anti-microbials. Method: Biofilm formation by SA in vitro was observed in detail using scanning electron microscopy. Approximately 500 substances were screened for a selective effect on SA growth and SA biofilm. Results: We found that xylitol inhibited the formation of glycocalyx, and farnesol dissolved fibrin fibers. Farnesol suppressed the growth of only SA, and did not affect that of SE. Xylitol and farnesol synergistically inhibited biofilm formation by SA. Conclusion: Xylitol and farnesol have potential for controlling the skin-microfloral balance because of their selective effects and inhibition of biofilm formation. They might provide a useful and safe method to care for skin colonized by SA, without using antibiotics.

Background: Seasonal changes affect the condition of skin and may trigger various cutaneous disorders. Objective: To clarify the effects of the environmental humidity on the skin pathology, we studied the effects of the humidity on a water-holding function of the stratum corneum. Methods: We evaluated the skin surface conductance, amino acid in the stratum corneum, and immunoreactivity of filaggrin of the epidermis of hairless mice kept in different environmental humidity. Results: Skin surface conductance in the stratum corneum of hairless mice 3–7 days after transfer from a humid environment (>80% relative humidity) to a dry (

Atopic dermatitis (AD), ichthyosis vulgaris (IV), and X-linked recessive ichthyosis (XLRI) are characterized by dry skin and impaired skin barrier. AD and IV are related to loss-of-function mutations in FLG (encoding filaggrin), whereas XLRI is caused by deletions or inactivating mutations in the steroid sulphatase gene (STS). Patients regularly use moisturizing creams, but little is known about the creams’ effects on the skin barrier.The present work combines objective scorings, non-invasive techniques, and molecular analyses of skin biopsies to characterize the skin in 57 patients with AD, IV, or XLRI, and in 14 healthy controls. Patients were classified according to their FLG and STS mutation status: AD with FLG+/+ (n = 14), AD with FLG+/– (n = 14), AD/IV with FLG–/– (n = 15), and XLRI with STS– (n = 14), as well as one man with a novel point mutation. Assessments were conducted at baseline and after four weeks of treatment with three different moisturizers applied to volar forearm skin.At baseline, dryness scoring and non-invasive assessments verified impaired skin barrier function in all patients. In patients with AD/IV, microarray analysis identified 300–3000 up- or downregulated mRNA transcripts involved in signalling pathways important for inflammation and barrier repair. The skin phenotype and number of altered transcripts were correlated with the FLG mutation status, with FLG–/– patients displaying the highest transepidermal water loss (TEWL) and the most altered transcript levels. In contrast, despite an equally dysfunctional skin barrier, only limited changes in mRNA transcripts occurred in XLRI patients. Treatment with moisturizers improved skin dryness similarly in all groups, but TEWL behaved differently: it decreased slightly in the AD/IV group and increased in the XLRI group, especially after urea treatment. Only minute effects on skin pH and mRNA expression were observed.In conclusion, FLG mutations elicit pro-inflammatory mechanisms probably aimed at restoring barrier competence. This does not occur in patients with XLRI, presumably because STS deficiency automatically increases the barrier thickness. Moisturizing treatment improves skin dryness in patients with AD, IV, or XLRI, but does not seem to normalize the altered epidermal gene expression profile in AD/IV patients.

Background Dietary milk phospholipids (MPLs) increase hydration of the stratum corneum and reduced transepidermal water loss (TEWL) in hairless mice fed a standard diet. However, the mechanism by which MPLs improve skin barrier functions has yet to be established. Objective This study was designed to examine the mechanism by which MPLs may affect covalently bound ceramides and markers of skin inflammation and improve the skin barrier defect in hairless mice fed a magnesium-deficient (HR-AD) diet. Methods Four-week-old female hairless mice were randomized into four groups (n = 10/group), and fed a standard (control) diet, the HR-AD diet, the HR-AD diet supplemented with either 7.0 g/kg MPLs (low [L]-MPL) or 41.0 g/kg MPLs (high [H]-MPL). Results Dietary MPLs improved the dry skin condition of hairless mice fed the HR-AD diet. MPLs significantly increased the percentage of covalently bound ω-hydroxy ceramides in the epidermis, and significantly decreased both thymus and activation-regulated chemokine (TARC) mRNA and thymic stromal lymphopoietin (TSLP) mRNA levels in skin, compared with the HR-AD diet. Furthermore, the MPL diets significantly decreased serum concentrations of immunoglobulin-E, TARC, TSLP, and soluble P-selectin versus the HR-AD diet. Conclusion Our study showed for the first time that dietary MPLs may modulate epidermal covalently bound ceramides associated with formation of lamellar structures and suppress skin inflammation, resulting in improved skin barrier function.

Although it has been well established that the dry skin often seen in patients with atopic dermatitis shows a deranged barrier function, there is no unanimity of opinion as to whether the barrier in normal-appearing skin of patients with the disease is deranged or not. Hence, it remains unclear whether individuals with atopic dermatitis constitution have an intrinsic derangement of skin barrier function or not. To settle this problem, in the present study we examined transepidermal water loss and stratum corneum water content in normal appearing skin of the upper back of 16 patients with completely healed atopic dermatitis who had been free from skin symptoms for 5 years or more, 30 patients with active atopic dermatitis, and 39 healthy subjects. The transepidermal water loss values and the stratum corneum water content values in normal-appearing skin of the completely healed patients were not different from the values in normal controls. These findings indicate that skin barrier function is not disturbed in patients with completely healed atopic dermatitis.

Glycosphingolipids including glucocerebroside (GluCer) and galactocerebroside (GalCer) have been recognized as bioreguratory lipids by our group and others. In addition, our recent study demonstrated that GalCer corrects dry skin conditions in humans. The processing of stratum corneum lipids, which occurs when beta-glucocerebrosidase (beta-GluCer'ase) changes GluCer to ceramide (Cer), is required to form the epidermal permeability barrier. We herein investigated the effects of GluCer, GalCer and Cer on the processing of GluCer to Cer by assaying epidermal beta-GluCer'ase in mice (155%, P < 0.01) when compared to vehicle treated controls, while neither GluCer nor Cer had this effect. Studies using inhibitors of beta-GluCer'ase or beta-galactosidase and measuring the optimum pH of the enzyme verified that GalCer specifically activated beta-GluCer'ase. We confirmed that GalCer significantly increased beta-GluCer'ase activity in the outer epidermal fraction (172%, P < 0.01) and that the activation of beta-GluCer'ase is not due to a direct activating effect of GalCer on the enzyme. Furthermore, the induction of beta-GluCer'ase activity by GalCer was also observed in cultured normal human deratinocytes (123%, P < 0.01). Finally, acylceramide content in stratum corneum was increased in mice treated with GalCer (194%, P < 0.0005). These results indicate that GalCer appears to affect the Cer construct in the stratum corneum by the activation of beta-GluCer'ase, which ultimately contribute to an enhancement of barrier formation.

Background Irritant contact dermatitis (ICD) is an inflammatory skin disease triggered by exposure to a chemical that is toxic or irritating to the skin. A major characteristic of chronic ICD is an inflammatory dry-skin condition with associated itching. Although glucosylceramide (GlcCer) is known to improve the skin barrier function, its mechanism of action is unknown. Objectives Using a mouse model of oxazolone-induced chronic ICD, this study investigated the effects of oral administration of GlcCer on inflammatory dry skin. Methods Chronic ICD was induced by repeated application of oxazolone in mice. GlcCer was orally administered once daily throughout the elicitation phase. The beneficial efficacy of GlcCer on cutaneous inflammation was evaluated by assessing ear thickness, lymph node weight, histological findings, and mRNA expression of pro-inflammatory cytokines such as IL-1β and IL-6. Additionally, parameters of the itch-associated response, including scratching behavior, water content of the skin, and aquaporin-3 levels in the lesional ear, were measured. Results Oral GlcCer administration significantly suppressed mRNA expression of the pro-inflammatory cytokines IL-1β and IL-6. GlcCer also suppressed ear swelling, lymph node weight gains, and infiltration of leukocytes and mast cells in ICD mice. In oxazolone-induced ICD mice, GlcCer significantly inhibited irritant-related scratching behavior and dehydration of the stratum corneum, and decreased aquaporin-3 expression. Conclusions Our results indicate that GlcCer suppressed inflammation not only by inhibiting cytokine production but also by repairing the skin barrier function, suggesting a potential beneficial role for GlcCer in the improvement of chronic ICD.

Background Serum thymus and activation-regulated chemokine (TARC) levels closely reflect the disease activity of atopic dermatitis (AD). AD is characterized by impaired epidermal barrier function and atopic dry skin. However, dry skin is also a very common problem in healthy individuals. Objective To investigate the relationship between serum TARC levels and epidermal barrier function in healthy subjects and patients with mild AD. Methods This study included 2 groups, 121 healthy subjects (healthy group) and 66 patients with mild AD (mild AD group). Barrier function was assessed by transepidermal water loss (TEWL) and stratum corneum hydration (SCH). Results Significantly elevated serum TARC levels and TEWL values and significantly decreased SCH values were detected in the mild AD group compared to those in the healthy group. In the mild AD group, serum TARC levels were significantly correlated with TEWL values and were inversely correlated with SCH values. Importantly, serum TARC levels were also inversely correlated with SCH values in the healthy controls. TEWL values in the healthy group tended to be correlated with TARC levels but did not reach statistical significance. Conclusion Together with TEWL and SCH, serum TARC level is a useful biomarker, reflecting impairment of epidermal function in AD patients as well as healthy subjects.

In common dermatoses, such as atopic dermatitis (AD), a decline in skin barrier function often accompanies an increased severity of clinical symptomatology, including pruritus [1]. Skin barrier disruption alters epidermal innervation and increases nerve density in the skin [2]. These findings are indicative of increases in sensory receptors responsive to exogenous trigger factors, suggesting that hyperinnervation is partly responsible for intense itch sensations [2]. Therefore, the abnormal innervation associated with skin barrier dysfunction such as dry skin has been considered as a target of antipruritic therapy. Moreover, recent studies have demonstrated that epidermal innervation is probably regulated by a fine balance of nerve elongation factors (e.g., nerve growth factor (NGF), amphiregulin, gelatinase) [2] and nerve repulsion factors (e.g., semaphorin 3A (Sema3A), anosmin-1) [2,3]. Although many people use emollients daily to alleviate symptoms of clinically and subjectively dry skin [4], the effects of emollients on nerve fiber density and nerve growth activity in dry skin remain unclear. We therefore examined the anti-nerve growth effects of petrolatum and heparinoid cream in the epidermis of acetone-treated mice, an animal model of acute dry skin [5].

Background UV-based therapy has anti-pruritic effects in inflammatory skin diseases, such as atopic dermatitis and psoriasis. These anti-pruritic effects may be partly due to inhibition of intraepidermal nerve growth, but they have not been fully characterized. Objective This study was performed to characterize the anti-nerve growth effects of UV-based therapies in acetone-treated mice as an acute dry skin model. Methods Nerve fibers penetrate into the epidermis 24 h after acetone treatment in mice, and nerve growth peaks 48 h after acetone treatment. To investigate the effects of UV-based therapies on the epidermal nerve fibers, including combination treatment with corticosteroid ointment, the mice were treated with psoralen ultraviolet A (PUVA), PUVA and betamethasone valerate ointment (PUVA + BV), narrowband ultraviolet B (NB-UVB), or an excimer lamp. Each therapy was provided 24 h after acetone treatment, and skin samples were taken 48 h later. Nerve fiber densities and expression levels of nerve growth factor (NGF) and semaphorin 3A (Sema3A) in the epidermis were examined by immunohistochemistry. Results Penetration of nerve fibers into the epidermis was observed in the acetone-treated mice, concomitant with increased NGF and decreased Sema3A levels in the epidermis. The acetone-induced intraepidermal nerve growth was significantly decreased by PUVA, PUVA + BV, NB-UVB, and excimer lamp treatments compared with controls. In addition, PUVA + BV and NB-UVB normalized the abnormal expression of NGF and Sema3A in the epidermis, but no such normalization was observed with excimer lamp treatment. Conclusion UV-based therapies, especially NB-UVB and excimer lamp treatments, may be effective therapeutic methods for pruritus involving epidermal hyperinnervation.

This comparative trial (histamine dry skin prick test versus control prick test) evaluates with subjective and objective clinical methods (i.e. itch scores, wheal area, and wheal and flare area) and with laser Doppler flowmetry (multiple sites measured between 5 and 15 min after prick test) the effect of increasing the duration of the skin prick (1, 3 and 10 s). As compared with control prick tests, all objective clinical parameters after histamine prick test were significantly different from the control prick tests. There was no interaction between agonist-duration of prick test and clinical parameters. When present, itch was reported only after histamine prick test. Skin blood perfusion values were evaluated with Laser Doppler flowmetry at prick test sites and at 1 cm distance from the prick test site. At control and histamine prick test sites, increased blood flow values were observed and a moderate interaction between agonist-duration of prick test and repeated measurement was noted (one tail P less than 0.05); there were indeed lower values 9 min after histamine prick tests whatever the duration of the prick test. At 1 cm distance from histamine prick test sites, all skin perfusion measurements (either 5-8 or 11-14 min) showed increased values over data recorded after control prick test (P less than 0.0001). On pooled data recorded at distance from histamine or control prick tests, there was a significant interaction between agonist-duration of prick test and laser Doppler flowmetry (P less than 0.0004).(ABSTRACT TRUNCATED AT 250 WORDS)

Summary Thymic stromal lymphopoietin (TSLP) is known for its capacity to induce CD11c+ myeloid dendritic cells to promote T helper type 2 (Th2)-skewed inflammatory responses. Although increased expression of TSLP was reported in the lesional skin of limited numbers of patients with atopic dermatitis (AD), the relationships between the degree of TSLP expression in the skin and the severity of AD, epidermal barrier function and eruption type remain to be elucidated. The aim of this study was to examine the relationships between the degree of TSLP expression in the skin and the severity of AD, eruption type and epidermal barrier function using a non-invasive method in a sizeable group of the patients. Stratum corneum tissue was obtained from AD patients by tape stripping, and the stratum corneum TSLP (scTSLP) expression level was evaluated using a TSLP-specific antibody followed by image analysis. The correlations between the scTSLP intensity and the severity scoring of AD (SCORAD) index and epidermal barrier function, such as stratum corneum hydration and transepidermal water loss (TEWL), were analysed. The changes in the scTSLP level induced by the application of moisturizer were also examined. The scTSLP expression level was increased in AD patients compared with healthy subjects and was correlated with SCORAD, especially with the dry skin score, and stratum corneum hydration. Moisturizer application resulted in reduced scTSLP levels. The scTSLP level can be used as a biomarker of AD severity and particularly epidermal barrier status.

Previous reports have demonstrated that stressful stimuli markedly influenced physiological conditions and homeostasis. In this study, we examined the influence of high population density environment on barrier function and water retention property of skin in mice. Overcrowding stress induced dramatic body weight reduction and significant increase in adrenal gland weight. Macroscopic skin appearance showed moderate exfoliation and slight wrinkle formation in the stress group. Moreover epidermis hyperplasia not concomitant with inflammatory reactions such as infiltration of immunocytes and vasodilation was observed in the skin from the stress group. Skin surface conductance in the stress group was significantly lower than in the control group. On the other hand, transepidermal water loss in the stress group increased significantly, compared to the control group. Moreover, transdermal penetration of indomethacin and nicotinic acid amide was enhanced significantly. These results suggest that overcrowding stress induced impairment of barrier function and water retention property. To elucidate the mechanism of overcrowding stress-induce dry skin, contents of ceramide and pyrrolidone carboxylic acid, which are the important compounds contributing to those functions were evaluated. Both of them in stratum corneum declined significantly in the stress group. Taken together, these results demonstrate that overcrowding stress induced dry skin, and that the impairment of barrier function and water retention property correlated with decrease in ceramide and pyrrolidone carboxylic acid.

Erratum to ‘‘Topical application of emollients prevents dry skin-inducible intraepidermal nerve growth in acetone-treated mice’’ [J. Dermatol. Sci. 62 (2011) 64–66] Atsuko Kamo , Mitsutoshi Tominaga , Osamu Negi , Suhandy Tengara , Hideoki Ogawa , Kenji Takamori * a Institute for Environmental and Gender Specific Medicine, Juntendo University Graduate School of Medicine, 2-1-1 Tomioka, Urayasu, Chiba 279-0021, Japan Department of Dermatology, Juntendo University Urayasu Hospital, 2-1-1 Tomioka, Urayasu, Chiba 279-0021, Japan