Expression of calcitonin gene-related peptide in atopic dermatitis and correlation with distress

Atopic dermatitis (AD) is a chronic, inflammatory, often severely itching skin disorder. It may worsen due to stress, depression, or anxiety. Calcitonin gene-related peptide (CGRP) may be involved in inflammation signaling. CGRP has also been suggested in relation to stress, depression, and anxiety....

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Published in:Immunopharmacology and immunotoxicology 2024, Vol.46 (1), p.67-72
Main Authors: Abdelhadi, Saly, Nordlind, Klas, Johansson, Björn, Theodorsson, Elvar, Holst, Mikael, Lönndahl, Louise
Format: Article
Language:English
Subjects:
Adult
Calcitonin Gene-Related Peptide - metabolism
Dermatitis, Atopic - pathology
Epidermis - pathology
Humans
Inflammation - pathology
Medicin och hälsovetenskap
Skin - pathology
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Summary:Atopic dermatitis (AD) is a chronic, inflammatory, often severely itching skin disorder. It may worsen due to stress, depression, or anxiety. Calcitonin gene-related peptide (CGRP) may be involved in inflammation signaling. CGRP has also been suggested in relation to stress, depression, and anxiety. This study aimed to investigate the expression of CGRP in the skin of patients with AD. Twenty-seven adult patients with AD, characterized with clinical and psychodemographic parameters, were investigated regarding CGRP expression in skin biopsies, using an immunohistochemical technique. The total number of CGRP-positive nerve-like fibers was found to be higher in lesional skin than in non-lesional skin. Moreover, more inflammatory cells of dendritic shape intruded into the epidermis in lesional skin compared to non-lesional skin. Keratinocytes showing expression of CGRP were also found in lesional skin. Interestingly, the number of CGRP-positive nerve-like fibers in lesional skin correlated with depressive and anxiety scores. Correlation with depressive score was also found for round CGRP-positive inflammatory cells in the epidermis. CGRP may have a role in both the inflammatory process and distress, in AD.
ISSN:0892-3973
1532-2513
1532-2513
DOI:10.1080/08923973.2023.2253988