We also investigated the inhibitory capacity of WIKIM30 on the development of 2,4-dinitrochlorobenzene-induced atopic dermatitis (AD), a Th2-dominant allergic disease in mice.Oral administration of <i>L. sakei</i> WIKIM30 significantly reduced AD-like skin lesions and serum immunoglobulin E and IL-4 levels while decreasing the number of CD4<sup>+</sup> T cells and B cells and the levels of Th2 cytokines (IL-4, IL-5, and IL-13) in peripheral lymph nodes and enhancing Treg differentiation and IL-10 secretion in mesenteric lymph nodes.
AD-MSCs showed an upregulation of many Th1/Th17 cytokines [interleukin (IL)-6, IL-8, IL-12, IL-13, IL-17A, IL-17F, transforming growth factor-β, interferon-γ], while Th2 chemokines (IL-2, IL-4, IL-5, IL-23A) were downregulated in AD-MSCs.
This study was designed to investigate mRNA expression of thymic stromal lymphopoietin (TSLP), thymus- and activation-regulated chemokine (TARC), interleukin-5 (IL-5), and IL-13 in AD before and after UVA1 therapy, to determine correlations among them, and to examine whether UVA1 influences their expression and whether it is associated with UVA1 efficacy.
Oral administration of L. chungangensis CAU 28(T) suppressed the production of IL-4, IL-5, IL-12, IFN-γ, tumor necrosis factor-α, and thymus- and activation-regulated chemokine (TARC) in skin lesions, indicating that it strongly drives the local immune system with efficacy comparable to that of tacrolimus, a topical immunomodulatory drug used for the treatment of atopic dermatitis.
We have shown that the resolution of extrinsic AE lesions following phototherapy is accompanied by significant reduction of mRNA expression of IL-5, IL-13 and IL-31, supporting current concepts that these cytokines play a crucial role in the pathogenesis of extrinsic AE and possibly represent targets for phototherapy.
We found that the rs2522411SNP and the haplotype T-A in the IL-5 gene and the serum IL-5 levels were strongly associated with the allergic type of AD, but not with the nonallergic type of AD.
Atopic dermatitis (AD) is a recurrent inflammatory skin disease characterized by high serum levels of IgE and Th2-type cytokines such as IL-4, IL-5 or IL-13.
To investigate the effects of tacrolimus on in vivo eosinophil counts and on the related molecules eotaxin, CCR3, RANTES and IL-5 in patients with atopic dermatitis (AD).
Azole derivatives, ketoconazole, itraconazole, miconazole, and nonazole terbinafine hydrochloride, and tolnaftate reduced interleukin-4 and interleukin-5 secretion without altering that of interferon-gamma and interleukin-2 in anti-CD3/CD28-stimulated T cells from both atopic dermatitis patients and normal donors.
The increased IL-5 and decreased IL-2 production observed with PBMCs from children with atopic dermatitis may underlie the activation of eosinophils and high serum immunoglobulin E concentrations also apparent in such individuals.
We demonstrated significant increases in IL-5 mRNA expression and protein production in different T cell fractions of children with allergic and non-allergic asthma and children with atopic dermatitis as compared to healthy controls.
These data indicate that although acute and chronic AD lesions are associated with increased activation of IL-4 and IL-5 genes, initiation of acute skin inflammation in AD is associated with a predominance of IL-4 expression whereas maintenance of chronic inflammation is predominantly associated with increased IL-5 expression and eosinophil infiltration.