Immunostimulatory Sequence CpG Elicits Th1-Type Immune Responses in Inflammatory Skin Lesions in an Atopic Dermatitis Murine Model

2008 ◽  
Vol 147 (1) ◽  
pp. 41-51 ◽  
Author(s):  
Guoying Wang ◽  
Nanna Fyhrquist-Vanni ◽  
Henrik Wolff ◽  
Marie-Caroline Dieu-Nosjean ◽  
Lajos Kemeny ◽  
...  
Author(s):  
Galina I. Smirnova

There are presented modern data describing the current understanding of the pathogenesis of atopic dermatitis (AD): a genetic predisposition to atopy, disruptions of epidermal barrier integrity and a cascade of immune responses, contributing allergic inflammation in the skin. There are both described several mechanisms of acute and chronic phases of AD, the main directions of pathogenetically substantiated treatment of AD in children and indicated the prospects of new preparations specific blockers of proinflammatory cytokines involved in the development of AD - crisaborole, apremilast, dupilumab, lebrikizumab, tralokinumab, tezepelumab. There is especially presented in details external therapy of atopic skin lesions in children with the use of means of modern dermatological cosmetics.


2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Yun-Zhu Li ◽  
Xue-Yan Lu ◽  
Wei Jiang ◽  
Lin-Feng Li

Qingpeng ointment (QP) is a Chinese medicine which has been used in treatment of atopic dermatitis (AD) in China. AD-like lesions were induced in BALB/c mice by repeated application of 2,4-dinitrofluorobenzene (DNFB) on shaved backs. The mice were then treated for 2 weeks with QP of different concentrations and Mometasone Furoate cream (MF), respectively. Macroscopic and microscopic changes of the skin lesions were observed after the treatment. The levels of serum immunoglobulin (Ig) E, tissue interferon (IFN)-γ, and interleukin (IL)-4 and IL-17A and the levels of involucrin, filaggrin, and kallikrein7 in epidermis were measured. The results show severe dermatitis with immune profiles similar to human acute AD. A significant infiltration of CD4+T and mast cells was observed in dermis of lesion but inhibited by QP after a 2-week treatment with it. The production of IgE, IL-4 and the mRNA expression of IL-17A were also suppressed, but the level of IFN-γwas increased. MF suppressed all production of these cytokines and IgE. Accordingly, the mechanism of QP on AD might correlate with its ability of modulating the immune dysfunctions rather than suppressing them. It had no effect on expressions of involucrin and filaggrin, except that its vehicle decreased the level of kallikrein7.


2011 ◽  
Vol 63 (3) ◽  
pp. 184-190 ◽  
Author(s):  
Tsuyoshi Mitsuishi ◽  
Kenji Kabashima ◽  
Hideaki Tanizaki ◽  
Ikuroh Ohsawa ◽  
Fumino Oda ◽  
...  

2017 ◽  
Vol 14 (4-5) ◽  
pp. 30-39
Author(s):  
G I Smirnova

Modern data describing the current understanding of the pathogenesis of atopic dermatitis (AD): a genetic predisposition to atopy, disturbances of the intestinal microbiome, disruptions of epidermal barrier integrity and a cascade of immune responses, contributing allergic inflammation in the skin are presented. There are both described several mechanisms of acute and chronic phases of AD, the main directions of pathogenetically substantiated treatment of AD in children and indicated the prospects of new preparations specific blockers of proinflammatory cytokines involved in the development of AD - crisaborole, dupilumab, apremilast et al. External therapy of atopic skin lesions in AD children with modern dermatological cosmetics is presented.


Pharmaceutics ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 750
Author(s):  
Ui Seok Kim ◽  
Jin Woo Park ◽  
Eon Sub Park ◽  
Joon Seok Bang ◽  
Tae Woo Jung ◽  
...  

This study aimed to restore the skin barrier function from atopic dermatitis (AD) via treatment with leucine-rich glioma inactivated 3 (LGI3) peptide. Male NC/Nga mice (7 weeks, 20 g) were randomly allocated into three groups (control, AD, and LGI3 group). After induction of AD skin lesions with Dermatophagoides farinae ointment, mice were treated with LGI3. The clinical score of AD was the highest and the dorsal skin thickness was the thickest in the AD group. In contrast, LGI3 treatment improved the clinical score and the dorsal skin thickness compared to the AD model. LGI3 treatment suppressed histopathological thickness of the epithelial cell layer of the dorsal skin. LGI3 treatment could indirectly reduce mast cell infiltration through restoring the barrier function of the skin. Additionally, the filaggrin expression was increased in immunohistochemical evaluation. In conclusion, the ameliorating effect and maintaining skin barrier homeostasis in the AD murine model treated with LGI3 could be attributed to complete re-epithelialization of keratinocytes. Hence, LGI3 might be considered as a new potential therapeutic target for restoring skin barrier function in AD.


2021 ◽  
Author(s):  
Zhiwen Zeng ◽  
Jinquan Huang ◽  
Yong Chen ◽  
Xiao Yu ◽  
Wei Zhu ◽  
...  

Abstract Objective Acupoint autohemotherapy (A-AHT) is considered an effective therapy for atopic dermatitis (AD) with few side-effects. Previous experiments showed the treatment had the potential to regulate T helper (Th) 1 and Th2 cytokines, like interferon (IFN)- gamma and interleukin (IL)- 4. This study focuses on the effects of A-AHT on the AD-like skin lesions through regulating Th1/Th2 immune responses. Methods The treatments of A-AHT, sham acupoint autohemotherapy and acupoint injection of normal saline were administered in the AD mice once every other day for 4 weeks. The total immunoglobulin (Ig) E, IL-4 and IFN-γ cytokine levels in the serum were examined after animal sacrifice. Th1/Th2 expression was analyzed in murine spleen cells via flow cytometry and immunohistochemical analysis of GATA-3 and T-bet in skin lesions were further assessed. Results Either type of repeated autologous whole blood (AWB) injection (into acupoint or sham acupoint) reduced the severity of AD-like symptoms and level of serum IgE. All of the three treatments had the similar inhibitory effect on levels of IL-4 and upregulation on the ratio of IFN-γ/IL-4, while differed on Th1/Th2 ratio as A-AHT regulates the body’s Th1/Th2 shift. This treatment also increased the related transcription factors T-bet expression, and upregulated T-bet/GATA3 ratio compared with the DNCB group. These differences were significant only in A-AHT group. Conclusion A-AHT effectively reduces AD symptoms and serum IgE levels in a mouse model and may act by regulating Th1/Th2 immune responses.


Sign in / Sign up

Export Citation Format

Share Document