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.

scholarly journals Mast Cell Deficient W/Wv Mice Lack Stress-Induced Increase in Serum IL-6 Levels, as Well as in Peripheral CRH and Vascular Permeability, a Model of Rheumatoid Arthritis

2002 ◽  
Vol 15 (3) ◽  
pp. 249-254 ◽  
Author(s):  
M. Huang ◽  
J. Berry ◽  
K. Kandere ◽  
M. Lytinas ◽  
K. Karalis ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Mast Cell ◽  
Mast Cells ◽  
Vascular Permeability ◽  
Acute Stress ◽  
Inflammatory Diseases ◽  
Joint Inflammation ◽  
Knee Joints ◽  
Deficient Mice ◽  
Wild Type Control

Corticotropin releasing hormone (CRH) and interleukin-6 (IL-6) are implicated in inflammatory diseases triggered by stress. Acute restraint stress increases serum IL-6 in the blood, but its source is not known. Our current study was carried out in order to determine the contribution of mast cells to stress-induced IL-6 release and to investigate skin CRH and vascular permeability in mice. W/Wv mast cell deficient and their wild type control +/+ mice were stressed in a plexiglass restraint chamber for 60 or 120 min. Serum corticosterone and IL-6 levels were measured. Other mice were injected with 99-Tchnetium gluceptate (99Tc) and its extravastion, indicating vascular permeability, was determined along with CRH levels in the skin and knee joints. Acute stress increased serum IL-6 in mice, but was greatly inhibited in W/Wv mast cell deficient mice. Vascular permeability to 99Tc, as well as local CRH levels, were also increased by stress, but not in W/Wv mice. Findings from our current study suggest a link between mast cells and stress-related skin and joint inflammation and may explain initial events in psoriatic and rheumatoid arthritis.

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.

Sign in / Sign up

Export Citation Format

Share Document