We investigated the potential effects of Costaria costata (CC) on atopic dermatitis (AD) development in chloro-2,4-dinitrobenzene (DNCB)-treated NC/Nga mice. CC is a brown alga distributed across the seas of Korea, China, and Japan. A total of 40 mice were randomly assigned to 5 groups with 8 mice per group: untreated Balb/c mice, AD control (0.1% w/v DNCB-treated NC/Nga mice), positive control (i.e., DNCB-treated NC/Nga mice fed a dietary supplement of 66.6 mg/kg of body weight [b.w.] of CJLP133), DNCB-treated NC/Nga mice fed a dietary supplement of 100 mg/kg b.w. of CCE10 (CCE10 100), and DNCB-treated mice fed a dietary supplement of 300 mg/kg b.w. of CCE10 (CCE10 300) groups. The CCE10 100 and CCE10 300 treatment groups suppressed AD development including clinical and histopathological changes and a reduction in skin hydration induced by DNCB. In addition, Th2 cytokine production in primary splenocytes, serum IgE and histamine production, and mast cell infiltration into the skin were suppressed in the CCE10 300 mice compared to the CCE10 100 mice. Our finding demonstrated an inhibitory effect of CCE10 in AD development by means of improving the Th1/Th2 cytokine balance and anti-inflammatory effect in an in vivo model.

Filaggrin (FLG) loss of function (LOF) variants are a major risk factor for the common inflammatory skin disease, atopic dermatitis (AD), and are often population-specific. African American (AA) children are disproportionately affected with AD, often later developing asthma and/or allergic rhinitis and comprise an atopy health disparity group for which the role of FLG LOF is not well known. Discovery of FLG LOF using exome sequencing is challenging given the known difficulties for accurate short-read alignment to FLG's high homology repeat variation. Here we employed an array-based sequencing approach to tile across each FLG repeat and discover FLG LOF in a well-characterized cohort of AA children with moderate to severe AD. Five FLG LOF were identified in 23% of our cohort. Two novel FLG LOF singletons, c.488delG and p.S3101*, were discovered as well as p.R501*, p.R826*, and p.S3316* previously reported for AD. p.S3316* (rs149484917) is likely an African ancestral FLG LOF, reported in African individuals in ExAC (Exome Aggregation Consortium), Exome Variant Server (ESP), and 4 African 1000G population databases (ESN, MSL, ASW, and ACB). The proportion of FLG LOF (11.5%) among the total FLG alleles in our cohort was significantly higher in comparisons to FLG LOF reported for African individuals in ExAC (2.5%; P = 4.3x10-4 ) and ESP (1.7%; P = 3.5x10-5 ) suggesting a disease-enrichment effect for FLG LOF. Our results demonstrate the utility of array-based sequencing in discovering FLG LOF, including novel and population-specific, that are of higher prevalence in our AA severe AD group than previously reported. This article is protected by copyright. All rights reserved.

We would like to thank Dr. Gaitanis and co-authors for their interest in our study. To date, many studies have investigated the role of the microbiome in chronic skin inflammatory diseases such as psoriasis and atopic dermatitis. M. restricta and globosa are the two main species of the all Malassezia yeast and the most common fungi on psoriatic skin. This article is protected by copyright. All rights reserved.

Atopic dermatitis is a chronic inflammatory skin disease caused by complex multifactorial etiology. In the recent years, there have been significant advances in tissue engineering and the generation of in vitro skin models representative of healthy and diseased states. This chapter describes the methodology for the fabrication of in vitro human skin equivalent (HSE) from human keratinocytes and fibroblasts using a fibrin-based dermal matrix and serum-free culture conditions. Modification of the culture conditions with the supplementation of Th2 cytokines such as interleukin-4 induces the development of atopic dermatitis-like skin model. The chapter also describes the histological and immunohistochemical tools for characterization of the HSE model. The reconstruction of tissue-engineered HSE models that recapitulate the essential features of atopic dermatitis provides powerful tools for deeper understanding of the underlying pathological mechanisms on epidermal level, identification and testing of novel treatment options, and safety and toxicological evaluation in a pathophysiologically relevant system.

Extensive studies support the presence of links between dyslipidemia and allergic diseases, and there has been with particular emphasis on allergen sensitization1-3 , asthma2,4 , and atopic dermatitis (AD). Although evidence supporting a link of allergic rhinitis (AR) with dyslipidemia is limited and controversial2,3 , many researchers have focused on the relationship of obesity and rhinitis, rather than blood lipids.5 This study determined the association of different blood lipids with current rhinitis and rhinitis-related parameters, including nasal symptoms, peripheral olfactory function, and nasal volume. This article is protected by copyright. All rights reserved.