Expression of endothelial and leukocyte adhesion molecules intercellular adhesion molecule-1, E-selectin, and vascular cell adhesion molecule-1 in the bronchial mucosa in steady-state and allergen-induced asthma

Bentley, Andrew; Durham, Stephen R.; Robinson, Douglas S.; Menz, G; Storz, Chr.; Cromwell, Oliver; Kay, A. B.; Wardlaw, Andrew J.

doi:10.1016/0091-6749(93)90064-m

Cited by 182 publications

(103 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Further support for this hypothesis stems from the results of in vivo studies in which ICAM-I and VCAM-1 monoclonal antibody therapy has proven effective in the treatment of T cell-mediated immune responses, such as arthritis (33) and transplantation (16,17), as well as in asthma (34) and repurfusion injury (35). While few such studies have been conducted on VCAM-1, the documented increased expression of this molecule in various human pathologies supports this notion (30,36,37).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of lymphocyte adhesion to cytokine‐activated synovial fibroblasts by glucocorticoids involves the attenuation of vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 gene expression

Tessier

Cattaruzzi

McColl

1996

Arthritis & Rheumatism

View full text Add to dashboard Cite

Objective. The aim of this study was to evaluate the ability of glucocorticoids to inhibit lymphocyte adhesion to human synovial fibroblasts. Methods. Adhesion of lymphocytes to cultured synovial fibroblasts was measured by counting the number of cells bound to fibroblasts. Surface expression of intercellular adhesion molecule 1 (ICAM‐1) was measured by enzyme‐linked immunosorbent assay, while vascular cell adhesion molecule 1 (VCAM‐1) surface expression was measured by flow cytometry. ICAM‐1 and VCAM‐1 messenger RNA (mRNA) levels were assessed by Northern blot analysis. Results. Stimulation of synovial fibroblasts by the proinflammatory cytokines tumor necrosis factor α, interleukin‐1β, and interferon‐γ resulted in a dose‐dependent increase in lymphocyte adhesion to synovial fibroblasts. This response was inhibited by preincubation of the cells with the synthetic glucocorticoid dexa‐methasone. Since lymphocyte adhesion to synovial fibroblasts is known to be mediated by VCAM‐1 and ICAM‐1, we examined the modulation of VCAM‐1 and ICAM‐1 expression in these cells. All 3 cytokines stimulated VCAM‐1 and ICAM‐1 surface and mRNA expression. Dexamethasone inhibited both VCAM‐1 and ICAM‐1 surface and mRNA expression in a dose‐dependent manner, which correlated with the inhibition of lymphocyte adhesion. Conclusion. Taken together, these results suggest that glucocorticoids may reduce inflammatory responses at extravascular sites by inhibiting the expression of these adhesion molecules, thereby reducing the adhesion of lymphocytes to connective tissue cells.

show abstract

Section: Discussionmentioning

confidence: 99%

Inhibition of lymphocyte adhesion to cytokine‐activated synovial fibroblasts by glucocorticoids involves the attenuation of vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 gene expression

Tessier

Cattaruzzi

McColl

1996

Arthritis & Rheumatism

View full text Add to dashboard Cite

show abstract

“…ICAM-1, VCAM-1 and E-selectin are constitutively expressed on the epithelium of the bronchial mucosa both in normal subjects and patients with either atopic or nonatopic asthma [72], but their expression is more pronounced in asthmatics than control subjects [73,76,79,80]. In patients with allergic asthma, a further significant increase in ICAM-1 expression occurs after allergen challenge [81].…”

Section: Icam-1 In Allergic Inflammation and Asthmamentioning

confidence: 99%

“…Several studies have shown prominent upregulation of ICAM-1 in asthmatic airways. Increased ICAM-1 expression in asthma has been reported on eosinophils [70], T-cells [71], and bronchial endothelial [72] and epithelial cells [73].…”

Section: Icam-1 In Allergic Inflammation and Asthmamentioning

confidence: 99%

The role of ICAM-1 on T-cells in the pathogenesis of asthma

Stanciu¹,

Djukanović²

1998

Eur Respir J

View full text Add to dashboard Cite

The capacity of inflammatory cells to adhere is critical to inflammatory responses and involves an array of adhesion molecules grouped into distinct families. Intercellular adhesion molecule (ICAM)-1 has recently attracted much interest in view of increasing evidence that it plays a prominent role in allergic diseases such as asthma and rhinitis. Apart from its role in adhesion of inflammatory cells to vascular endothelium, the extracellular matrix and epithelium, ICAM-1 mediates T-cell/T-cell, T-cell/target cell and T-cell/B-cell interactions. ICAM-1 on the surface of T-cells is thought to participate in signal transduction and may thus modulate several functions including activation, proliferation, cytotoxicity and cytokine production. Because ICAM-1 is the receptor for the major group of rhinoviruses, the most important cause of acute asthma attacks, binding of rhinovirus (RV) to ICAM-1 on T-cells may, at least theoretically, modulate their function. We review here the role of ICAM-1 in asthma and focus more specifically on its expression on T-cells. We present evidence for a general increase in ICAM-1 expression in this disease including recent observations of enhanced expression on the surface of T-cells in the airways lumen. Whilst the implications of intercellular adhesion molecule- upregulation in asthma remain to be fully elucidated, its participation in cell trafficking and activation are being considered as a target for treatment. We present here early attempts to interfere with intercellular adhesion molecule-1 as an adhesion molecule involved in cell influx and studies aimed preventing virus-induced exacerbations of asthma in children based on the knowledge that intercellular adhesion molecule-1 is the receptor for rhinoviruses.

show abstract

“…This may be important for allergic inflammatory responses since it is a receptor for VCAM-1, and correlations have been found between infiltration of eosinophils and expression of VCAM-1 in the lungs of patients with asthma as well as in late phase reactions in the lungs, nose or skin (Kyan-Aung et al 1991, Bentley et al 1993, Lee et al 1994, Gosset et al 1994, Ohkawara et al 1995, Fukuda et al 1996. Expression of VCAM-1 also correlated with eosinophil numbers in nasal polyp tissues (Jahnsen et al 1995, Beck et al 1996.…”

Section: Eosinophil-endothelial Interactionsmentioning

confidence: 99%