scholarly journals Mast Cells Limit Ear Swelling Independently of the Chymase Mouse Mast Cell Protease 4 in an MC903-Induced Atopic Dermatitis-Like Mouse Model

2020 ◽  
Vol 21 (17) ◽  
pp. 6311
Author(s):  
Sofie Svanberg ◽  
Zhiqiang Li ◽  
Pontus Öhlund ◽  
Ananya Roy ◽  
Magnus Åbrink
Keyword(s):  
Atopic Dermatitis ◽  
Mast Cells ◽  
Clinical Score ◽  
Serum Levels ◽  
Mouse Strains ◽  
Interleukin 33 ◽  
Tissue Levels ◽  
Granulocyte Infiltration ◽  
Protease Deficient ◽  
Mouse Mast Cell

Atopic dermatitis (AD) is a complex, often lifelong allergic disease with severe pruritus affecting around 10% of both humans and dogs. To investigate the role of mast cells (MCs) and MC-specific proteases on the immunopathogenesis of AD, a vitamin D3-analog (MC903) was used to induce clinical AD-like symptoms in c-kit-dependent MC-deficient Wsh−/− and the MC protease-deficient mMCP-4−/−, mMCP-6−/−, and CPA3−/− mouse strains. MC903-treatment on the ear lobe increased clinical scores and ear-thickening, along with increased MC and granulocyte infiltration and activity, as well as increased levels of interleukin 33 (IL-33) locally and thymic stromal lymphopoietin (TSLP) both locally and systemically. The MC-deficient Wsh−/− mice showed significantly increased clinical score and ear thickening albeit having lower ear tissue levels of IL-33 and TSLP as well as lower serum levels of TSLP as compared to the WT mice. In contrast, although having significantly increased IL-33 ear tissue levels the chymase-deficient mMCP-4−/− mice showed similar clinical score, ear thickening, and TSLP levels in ear tissue and serum as the WT mice, whereas mMCP-6 and CPA3 -deficient mice showed a slightly reduced ear thickening and granulocyte infiltration. Our results suggest that MCs promote and control the level of MC903-induced AD-like inflammation.

scholarly journals Η επίδραση του stress στην έκφραση των υποδοχέων του CRH και τα επίπεδά του σε ασθενείς με σύνδρομο ατοπικού εκζέματος / δερματίτιδος, χρόνιας κνίδωσης και ψωρίασης

2012 ◽  
Author(s):  
Μαγδαληνή Βασιάδη
Keyword(s):  
Atopic Dermatitis ◽  
Mast Cells ◽  
Vascular Permeability ◽  
Chronic Urticaria ◽  
Acute Stress ◽  
Serum Levels ◽  
Releasing Hormone ◽  
Level Increase ◽  
Skin Biopsies ◽  
Permeability Increase

The goal of this study is to investigate mast cells role in inflammatory skin disorders that worsen by stress, like atopic dermatitis, chronic urticaria kai psoriasis. Specifically, human samples are used to analyze the expression and the effect of corticotropin releasing hormone (CRH) and its receptors on the stimulation of skin mast cells and the vascular permeability increase. The hypothesis is that in these diseases acute stress causes CRH release systematically or topically on the skin, which either alone or in combination with substance P (SP) or neurotensin (NT) release, causes mast cells activation, leading to vascular permeability increase and neurogenic inflammation.The hypothesis above is built on important preliminary results that our team has published in the past. CRH receptors expression was studied human skin biopsies from patients with atopic dermatitis, chronic urticaria and psoriasis, using quantitative Real Time-PCR (qRT-PCR), while CRH, NT and VEGF serum levels were measured using ELISA or milliplex technology. Finally, State-Trait Anxiety Inventory questionnaire (STAI) was used to draw correlations between findings and stress levels.Data show statistically significant serum CRH increase in atopic dermatitis and psoriasis, while there is a statistically significant decrease in corticotrophin releasing hormone receptor 1 (CRHR-R1) in lesion skin of the same patients. Statistical analysis of a small group of patients, which filled in STAI, showed correlation between stress level and serum CRH levels. Moreover, serum NT and VEGF levels were statistically significant higher. A possible explanation would be acute stress to cause serum CRH level increase, subsequent CRH-R1 down-regulation topically in the skin, following by synergistic action of CRH and NT to cause vascular permeability increase.

Increased serum levels of interleukin 33 in patients with atopic dermatitis

2014 ◽  
Vol 70 (5) ◽  
pp. 882-888 ◽  
Author(s):  
Risa Tamagawa-Mineoka ◽  
Yasutaro Okuzawa ◽  
Koji Masuda ◽  
Norito Katoh
Keyword(s):  
Atopic Dermatitis ◽  
Serum Levels ◽  
Interleukin 33

Mast cell-nerve fiber interaction: Ultrastructural studies

1990 ◽  
Vol 48 (3) ◽  
pp. 428-429
Author(s):  
E.Y. Chi ◽  
M.L. Su ◽  
Y.T. Tien ◽  
W.R. Henderson
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Substance P ◽  
Nerve Fiber ◽  
Sensory Nerves ◽  
Ultrastructural Studies ◽  
Morphological Studies ◽  
Granulocyte Infiltration ◽  
Intracutaneous Injection ◽  
Recent Attention

Recent attention has been directed to the interaction of the nerve and immune systems. The neuropeptide substance P, a tachykinnin which is a neurotransmitter in the central and peripheral nervous systems produces tissue swelling, augemntation of intersitial fibrin deposition and leukocyte infiltration after intracutaneous injection. There is a direct correlation reported between the extent of mast cell degranulation at the sites of injection and the tissue swelling or granulocyte infiltration. It has previously been demonstrated that antidromic electrical stimulation of sensory nerves induces degranulation of cutaneous mast cells, cutaneous vasodilation and augmented vascular permeability. Morphological studies have documented a close anatiomical association between mast cells and nonmyelinated nerves, that contain substance P and other neuropeptides. However, the presence of mast cells within nerve fasicles has not been previously examined ultrastructurally. In this study, we examined ultrastructurally the distribution of mast cells in the nerve fiber bundles located in the muscular connective tissue of rat tongues (n=20).

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 Lack of interleukin-33 and its receptor does not prevent calcipotriol-induced atopic dermatitis-like inflammation in mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Wojciech Pietka ◽  
Olav Sundnes ◽  
Clara Hammarström ◽  
Manuela Zucknick ◽  
Denis Khnykin ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Interleukin 33

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.

Sign in / Sign up

Export Citation Format

Share Document