Endothelial leucocyte adhesion molecule-1 (ELAM-1) expression in cutaneous inflammation

Abstract

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-alpha) 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-gamma (30 micrograms) 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 be 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.

Stress-induced enhancement of skin immune function: A role for γ interferon

“…5 suggest that IFN␥ may also mediate a stress-induced enhancement of skin DTH by enhancing the recruitment, activation, and͞or effector function of leukocytes. With respect to leukocyte recruitment, numerous studies have shown that intradermal administration of IFN␥ to normal human skin (in doses similar to those applied in our studies) induces a significant increase in the expression of cell adhesion molecules, such as L-selectin (CD62-L), lymphocyte function-associated antigen (LFA-1), and intercellular adhesion molecule (ICAM-1), on endothelial cells (49,50), leukocytes (51,52), and keratinocytes (53), with ICAM-1 expression occurring first on endothelial cells and later on keratinocytes (54). With respect to leukocyte activation, low levels of corticosterone have been shown to potently enhance the early stages of T cell activation and T lymphocyte proliferation (55).…”

MicroRNA-31 Is Overexpressed in Psoriasis and Modulates Inflammatory Cytokine and Chemokine Production in Keratinocytes via Targeting Serine/Threonine Kinase 40

“…The first step of recruitment of leukocytes to the skin is the attachment of circulating cells to vascular endothelial cells, which is mediated by cell adhesion molecules, such as ICAM-1, VCAM-1, and Eselectin (21). It has been shown that the expression of these cell adhesion molecules is increased on dermal vessels of psoriatic skin (22)(23)(24)(25). To test the effect of miR-31 on endothelial cell-activating capacity of keratinocytes, we measured the expressions of ICAM-1, VCAM-1, and E-selectin in primary HUVECs incubated with culture medium from miR-31 inhibitor-treated keratinocytes.…”

Differences in leucocyte-endothelium interactions between normal and adenocarcinoma bearing tissues in response to radiation

“…For example, a report by Ohkubo et al (1991) indicated that, under control conditions, leucocyte adhesion to microvascular endothelium in VX2 carcinoma was lower than that in normal tissues. Groves et al (1991) reported that while the expression Eselectin was present on the endothelial cells of squamous cell carcinomas, it was undetectable on vessels of basal cell carcinoma. Kuzu et al (1993) reported that the expression of several important adhesion molecules for leucocyte adhesion (i.e.…”