Mast Cells in Atopic Dermatitis: Resistance against Medium-Dose UVA1 Phototherapy?

Dermatology ◽  
2003 ◽  
Vol 207 (3) ◽  
pp. 334-336
Author(s):  
F. Breuckmann ◽  
G. von Kobyletzki ◽  
A. Avermaete ◽  
A. Kreuter ◽  
P. Altmeyer ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Mast Cells ◽  
Uva1 Phototherapy ◽  
Medium Dose

scholarly journals A medium dose of UVA1 phototherapy does not diminish vitamin D level in patients with atopic dermatitis

2020 ◽  
Vol 107 (2) ◽  
pp. 148-158
Author(s):  
Małgorzata Bernacka ◽  
Anna Woźniacka ◽  
Karolina Malinowska ◽  
Jarosław Bogaczewicz
Keyword(s):  
Vitamin D ◽  
Atopic Dermatitis ◽  
Uva1 Phototherapy ◽  
Medium Dose

scholarly journals ‘High dose’ vs. ‘medium dose’ UVA1 phototherapy in italian patients with severe atopic dermatitis

2018 ◽  
Vol 33 (4) ◽  
pp. 718-724 ◽  
Author(s):  
A. Pacifico ◽  
P. Iacovelli ◽  
G. Damiani ◽  
C. Ferraro ◽  
S. Cazzaniga ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Severe Atopic Dermatitis ◽  
High Dose ◽  
Uva1 Phototherapy ◽  
Medium Dose

Long-term efficacy of medium-dose UVA1 phototherapy in atopic dermatitis☆, ☆☆

2000 ◽  
Vol 42 (2) ◽  
pp. 254-257 ◽  
Author(s):  
D ABECK ◽  
T SCHMIDT ◽  
H FESQ ◽  
K STROM ◽  
M MEMPEL ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Term Efficacy ◽  
Uva1 Phototherapy ◽  
Medium Dose

High-dose versus medium-dose UVA1 phototherapy for patients with severe generalized atopic dermatitis

2001 ◽  
Vol 45 (4) ◽  
pp. 503-507 ◽  
Author(s):  
Stanislava Tzaneva ◽  
Arno Seeber ◽  
Martina Schwaiger ◽  
Herbert Hönigsmann ◽  
Adrian Tanew
Keyword(s):  
Atopic Dermatitis ◽  
High Dose ◽  
Uva1 Phototherapy ◽  
Medium Dose

scholarly journals Modulation of cathepsin G expression in severe atopic dermatitis following medium-dose UVA1 phototherapy

2002 ◽  
Vol 2 (1) ◽  
Author(s):  
Frank Breuckmann ◽  
Gregor von Kobyletzki ◽  
Annelies Avermaete ◽  
Alexander Kreuter ◽  
Peter Altmeyer ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Cathepsin G ◽  
Severe Atopic Dermatitis ◽  
Uva1 Phototherapy ◽  
Medium Dose

scholarly journals Gut microbiota restoration through fecal microbiota transplantation: a new atopic dermatitis therapy

2021 ◽  
Author(s):  
Jong-Hwa Kim ◽  
Kiyoung Kim ◽  
Wonyong Kim
Keyword(s):  
Atopic Dermatitis ◽  
Mast Cells ◽  
Gut Microbiota ◽  
Immune Modulation ◽  
Fecal Microbiota Transplantation ◽  
Blood Parameters ◽  
Fecal Microbiota ◽  
Th1 And Th2 Cytokines ◽  
Calprotectin Level ◽  
Donor State

AbstractThe pathogenesis of atopic dermatitis (AD) involves complex factors, including gut microbiota and immune modulation, which remain poorly understood. The aim of this study was to restore gut microbiota via fecal microbiota transplantation (FMT) to ameliorate AD in mice. FMT was performed using stool from donor mice. The gut microbiota was characterized via 16S rRNA sequencing and analyzed using Quantitative Insights into Microbial Ecology 2 with the DADA2 plugin. Gut metabolite levels were determined by measuring fecal short-chain fatty acid (SCFA) contents. AD-induced allergic responses were evaluated by analyzing blood parameters (IgE levels and eosinophil percentage, eosinophil count, basophil percentage, and monocyte percentage), the levels of Th1 and Th2 cytokines, dermatitis score, and the number of mast cells in the ileum and skin tissues. Calprotectin level was measured to assess gut inflammation after FMT. FMT resulted in the restoration of gut microbiota to the donor state and increases in the levels of SCFAs as gut metabolites. In addition, FMT restored the Th1/Th2 balance, modulated Tregs through gut microbiota, and reduced IgE levels and the numbers of mast cells, eosinophils, and basophils. FMT is associated with restoration of gut microbiota and immunologic balance (Th1/Th2) along with suppression of AD-induced allergic responses and is thus a potential new therapy for AD.

scholarly journals Ubiquitous Overexpression of Chromatin Remodeling Factor SRG3 Exacerbates Atopic Dermatitis in NC/Nga Mice by Enhancing Th2 Immune Responses

2021 ◽  
Vol 22 (4) ◽  
pp. 1553
Author(s):  
Sung Won Lee ◽  
Hyun Jung Park ◽  
Jungmin Jeon ◽  
Yun Hoo Park ◽  
Tae-Cheol Kim ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Mast Cells ◽  
Immune Responses ◽  
Chromatin Remodeling ◽  
Skin Diseases ◽  
Immunoglobulin E ◽  
Critical Role ◽  
Interleukin 4 ◽  
Inflammatory Skin Diseases ◽  
Immune Disorder

The SWItch (SWI)3-related gene (SRG3) product, a SWI/Sucrose Non-Fermenting (SNF) chromatin remodeling subunit, plays a critical role in regulating immune responses. We have previously shown that ubiquitous SRG3 overexpression attenuates the progression of Th1/Th17-mediated experimental autoimmune encephalomyelitis. However, it is unclear whether SRG3 overexpression can affect the pathogenesis of inflammatory skin diseases such as atopic dermatitis (AD), a Th2-type immune disorder. Thus, to elucidate the effects of SRG3 overexpression in AD development, we bred NC/Nga (NC) mice with transgenic mice where SRG3 expression is driven by the β-actin promoter (SRG3β-actin mice). We found that SRG3β-actin NC mice exhibit increased AD development (e.g., a higher clinical score, immunoglobulin E (IgE) hyperproduction, and an increased number of infiltrated mast cells and basophils in skin lesions) compared with wild-type NC mice. Moreover, the severity of AD pathogenesis in SRG3β-actin NC mice correlated with expansion of interleukin 4 (IL4)-producing basophils and mast cells, and M2 macrophages. Furthermore, this accelerated AD development is strongly associated with Treg cell suppression. Collectively, our results have identified that modulation of SRG3 function can be applied as one of the options to control AD pathogenesis.

scholarly journals Topical Spilanthol Inhibits MAPK Signaling and Ameliorates Allergic Inflammation in DNCB-Induced Atopic Dermatitis in Mice

2019 ◽  
Vol 20 (10) ◽  
pp. 2490 ◽  
Author(s):  
Wen-Chung Huang ◽  
Chun-Hsun Huang ◽  
Sindy Hu ◽  
Hui-Ling Peng ◽  
Shu-Ju Wu
Keyword(s):  
Atopic Dermatitis ◽  
Mast Cells ◽  
Protein Kinase ◽  
Allergic Inflammation ◽  
Skin Lesions ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Mapk Pathways ◽  
Mitogen Activated Protein ◽  
Cox 2

Atopic dermatitis (AD) is a recurrent allergic skin disease caused by genetic and environmental factors. Patients with AD may experience immune imbalance, increased levels of mast cells, immunoglobulin (Ig) E and pro-inflammatory factors (Cyclooxygenase, COX-2 and inducible NO synthase, iNOS). While spilanthol (SP) has anti-inflammatory and analgesic activities, its effect on AD remains to be explored. To develop a new means of SP, inflammation-related symptoms of AD were alleviated, and 2,4-dinitrochlorobenzene (DNCB) was used to induce AD-like skin lesions in BALB/c mice. Histopathological analysis was used to examine mast cells and eosinophils infiltration in AD-like skin lesions. The levels of IgE, IgG1 and IgG2a were measured by enzyme-linked immunosorbent assay (ELISA) kits. Western blot was used for analysis of the mitogen-activated protein kinase (MAPK) pathways and COX-2 and iNOS protein expression. Topical SP treatment reduced serum IgE and IgG2a levels and suppressed COX-2 and iNOS expression via blocked mitogen-activated protein kinase (MAPK) pathways in DNCB-induced AD-like lesions. Histopathological examination revealed that SP reduced epidermal thickness and collagen accumulation and inhibited mast cells and eosinophils infiltration into the AD-like lesions skin. These results indicate that SP may protect against AD skin lesions through inhibited MAPK signaling pathways and may diminish the infiltration of inflammatory cells to block allergic inflammation.

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