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

Abstract

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.