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Atopic dermatitis (AD) is a common chronic inflammatory skin disease with a high prevalence worldwide, including countries from Asia, Africa, and Latin America, and in different ethnic groups. In recent years, more attention has been placed on the heterogeneity of AD associated with multiple factors, including a patient's ethnic background, resulting in an increasing body of clinical, genetic, epidemiologic, and immune-phenotypic evidence that delineates differences in AD among racial groups. Filaggrin (FLG) mutations, the strongest genetic risk factor for the development of AD, are detected in up to 50% of European and 27% of Asian AD patients, but very rarely in Africans. Th2 hyperactivation is a common attribute of all ethnic groups, though the Asian endotype of AD is also characterized by an increased Th17-mediated signal, whereas African Americans show a strong Th2/Th22 signature and an absence of Th1/Th17 skewing. In addition, the ethnic heterogeneity of AD may hold important therapeutic implications as a patient's genetic predisposition may affect treatment response and, thereby, a tailored strategy that better targets the dominant immunologic pathways in each ethnic subgroup may be envisaged. Nevertheless, white patients with AD represent the largest ethnicity enrolled and tested in clinical trials and the most treated in a real-world setting, limiting investigations about safety and efficacy across different ethnicities. The purpose of this review is to describe the heterogeneity in the pathophysiology of AD across ethnicities and its potential therapeutic implications. [ABSTRACT FROM AUTHOR]

Angelicae tenussimae root has been used as a traditional medicine in Asia. Recently, anti-melanogenic and anti-photogenic effects of fermented A. tenuissima root (FAT) were identified. However, information about the anti-atopic dermatitis action of FAT is limited. Thus, the purpose of this study is to determine the applicability of FAT to AD by identifying the efficacy of FAT on the skin barrier and inflammatory response, which are the main pathogenesis of AD. Expression levels of skin barrier components and the production of inflammatory mediators in human keratinocyte and mouse macrophage cells were measured by quantitative RT-PCR or ELISA. FAT upregulated the expression of skin barrier components (filaggrin, involucrin, loricurin, SPTLC1) and inhibited the secretion of an inflammatory chemokine TARC in HaCaT cells. Furthermore, it suppressed pro-inflammatory cytokines (IL-6, TNF-α) and nitric oxide production in LPS-induced RAW264.7 cells. In addition, ligustilide increased filaggrin and SPTLC1, and also lowered pro-inflammatory mediators that increased in atopic environments, such as in FAT results. This means that ligustilide, one of the active ingredients derived from FAT, can ameliorate AD, at least in part, by promoting skin barrier formation and downregulating inflammatory mediators. These results suggest that FAT is a potential functional cosmetic material for the care and management of AD. [ABSTRACT FROM AUTHOR]

Grewia tomentosa Juss. is a deciduous shrub that mainly grows in Asia. Despite studies of other Grewia species for treatment of various diseases, Grewia tomentosa Juss. has not been studied as a medicinal herb. This study evaluates the anti-allergic and anti-topic dermatitis activity of Grewia tomentosa Juss. ethanol extract (Gt-EE). The results show that Gt-EE suppressed IgE–antigen-induced β-hexosaminidase release. The mRNA expression of IL-1β, IL-4, IL-5, IL-6, IL-13, TNF-α, MCP-1, and TSLP, which are involved in allergic responses, was inhibited by Gt-EE in IgE-stimulated RBL-2H3 cells. In addition, the phosphorylation of Syk, PLCγ1, PKCδ, PI3K, AKT, NF-κB p65, NF-κB p50, p38, JNK, and ERK1/2 was decreased by Gt-EE in these cells. Gt-EE also showed anti-inflammatory effects in in vivo mouse models. In passive cutaneous anaphylaxis (PCA), a commonly used mouse model, Gt-EE decreased the allergic response, infiltration of mast cells, and mRNA level of IL-4. Furthermore, Gt-EE ameliorated symptoms of DNCB-induced atopic dermatitis (AD). In DNCB-induced AD, Gt-EE suppressed the increase in mast cells, serum IgE level, expression of allergic mediators (IL-1β, IL-4, IL-5, IL-6, TNF-α), and phosphorylation of proteins (IκBα, NF-κB p65, NF-κB p50, p38, JNK, and ERK1/2) implicated in allergic reactions [ABSTRACT FROM AUTHOR]