CGRP-immunoreactive nerves in prurigo nodularis - an exploration of neurogenic inflammation

Background: The present study has explored the localization and distribution of calcitonin gene‐related peptide (CGRP)‐immunoreactive (IR) nerve fibers in prurigo nodularis, especially emphasizing its relationships to mast cells and eosinophils, which all are important contributors to inflammation....

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Published inJournal of cutaneous pathology Vol. 27; no. 7; pp. 359 - 366
Main Authors Liang, Yong, Jacobi, Henrik H., Reimert, Claus M., Haak-Frendscho, Mary, Marcusson, Jan A., Johansson, Olle
Format Journal Article
LanguageEnglish
Published Copenhagen Munksgaard International Publishers 01.08.2000
Blackwell
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Summary:Background: The present study has explored the localization and distribution of calcitonin gene‐related peptide (CGRP)‐immunoreactive (IR) nerve fibers in prurigo nodularis, especially emphasizing its relationships to mast cells and eosinophils, which all are important contributors to inflammation. Methods: The exact localization of CGRP in the nerve fibers of prurigo nodularis lesional skin has been clarified by an ultrastructural immunogold labelling technique; and the relationships of CGRP‐IR nerve fibers to tryptase‐IR mast cells or eosinophil cationic protein (ECP)‐IR eosinophils were also investigated by immunofluorescence double‐labelling. Results: This ultrastructural study has demonstrated that CGRP immunoreactivity is increased in the dense‐core vesicles in the axons of the prurigo nodularis lesional skin; the axons which contain CGRP are, in addition, enlarged and have more dense‐core vesicles than the axons which do not contain CGRP. The immunofluorescence investigation demonstrated that tryptase‐containing mast cells and ECP‐containing eosinophils also are significantly increased in the lesional skin. Conclusions: The results indicate that certain neurons increasingly express CGRP, which may dynamically result in a neurogenic inflammation in the lesional skin, through vasodilatation, and recruitment and regulation of inflammatory cells, e.g. eosinophils and mast cells.
Bibliography:ark:/67375/WNG-V62MVH3P-M
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ArticleID:CUP27007359
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content type line 23
ISSN:0303-6987
1600-0560
DOI:10.1034/j.1600-0560.2000.027007359.x