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Adhesion molecules in atopic dermatitis: VCAM‐1 and ICAM‐1 expression is increased in healthy‐appearing skin
Author(s) -
Jung K.,
Linse F.,
Heller R.,
Moths C.,
Goebel R.,
Neumann Ch.
Publication year - 1996
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.1996.tb04651.x
Subject(s) - cell adhesion molecule , atopic dermatitis , vcam 1 , intercellular adhesion molecule 1 , downregulation and upregulation , immunology , icam 1 , e selectin , medicine , immunostaining , cd31 , inflammation , cell adhesion , adhesion , pathology , biology , chemistry , immunohistochemistry , biochemistry , organic chemistry , gene
In the skin of normal and atopic individuals, the expression of E‐selecting (ELAM‐l), L‐selectin (LECAM‐l), P‐selection (CD62), CD31 (PECAM), vascular cell adhesion molecule‐1 (VCAM‐l), intercellular adhesion molecule‐1 (ICAM‐l), and cutaneous lymphocyte antigen (CLA) were compared by immunostaining of skin biopsies which were taken from normal individuals ( n = 17), the healthy‐appearing skin of patients with atopic dermatitis ( n = lo), and their acute ( n = 5) and chronic (n = 6) skin lesions. In contrast to ELAM‐1, the expression of VCAM‐1 and ICAM‐1 was found to be significantly increased in non lesional atopic skin in comparison to the skin of normal individuals. Moreover, in contrast to normal skin of healthy individuals, nonlesional atopic skin showed a further increase of VCAM‐1, ICAM‐1, and ELAM‐1 when cultured with medium alone. This suggests that certain adhesion molecules are constitutively upregulated in healthy‐appearing skin of patients with atopic dermatitis. In addition, atopic skin appears to respond to nonspecific stimuli (such as culture with medium alone) with upregulation of VCAM‐1, ICAM‐1, and ELAM‐1. It is suggested that the observed upregulation of adhesion molecules is mediated by the release of cytokines such as interleukin‐4 from cells which reside in atopic skin. The question of whether the inherent up regulation of adhesion molecules in atopic skin contributes to the development of Th2 cells, which have been found to predominate in atopic inflammation, has to be further investigated.