Premium
Endothelial leucocyte adhesion molecule‐1 (ELAM‐1) expression in cutaneous inflammation
Author(s) -
GROVES R. W.,
ALLEN M. H.,
BARKER J. N. W. N.,
HASKARD D. O.,
MACDONALD D. M.
Publication year - 1991
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.1991.tb00419.x
Subject(s) - intercellular adhesion molecule 1 , cytokine , endothelium , cell adhesion molecule , e selectin , inflammation , tumor necrosis factor alpha , peripheral blood mononuclear cell , medicine , pathology , immunology , keratinocyte , biology , cell adhesion , adhesion , in vitro , chemistry , biochemistry , organic chemistry
Summary Endothelial leucocyte adhesion molecule‐1 (ELAM‐1) is a recently described endothelial surface glycoprotein which is inducible by interleukin 1 (IL‐1). tumour necrosis factor‐alpha (TNF‐α) or bacterial lipopolysaccharide (LPS). Using an immunohistochemical technique and a monoclonal antibody (1.2B6) specific for ELAM‐1 we have found marked vascular endothelial expression of ELAM‐1 in many cutaneous inflammatory disorders, including allergic contact dermatitis, atopic dermatitis and psoriasis, and in dermal infiltrates associated with benign, premalignant and malignant keratinocyte proliferation. In normal skin, minimal levels of ELAM‐1 expression were detected. In psoriasis, double immunoenzyme staining studies revealed a close spatial relationship between ELAM‐1 expression and neutrophil margination, suggesting a functional link. Recombinant human interferon‐7 (30 μg) injected intradermally in normal adult human volunteers did not substantially upregulate ELAM‐1 in contrast to its marked effect on intercellular adhesion molecule‐1 (ICAM‐1) expression, indicating that this cytokine is probably not involved in ELAM‐1 induction in vivo. These results indicate that ELAM‐1 is widely induced in cutaneous inflammation with a time course of expression that is longer than that observed in vitro . As ELAM‐1 acts as an adhesion ligand for neutrophils. and perhaps monocytes. the expression of this molecule in cutaneous lesions is likely to he an indication of the ability of vascular endothelium to recruit these cells from the circulation. Furthermore, the cytokine inducibility of ELAM‐1 is indirect evidence for functional interactions between perivascular mononuclear cells, other resident cells and the blood vessel wall.