285 Bronchial mucosal intercellular adhesion molecule-1 [ICAM-1] and endothelial leukocyte adhesion molecule-1 [ELAM-1] expression in normals and asthmatics

Montefort, Stephen; Howarth, Peter H.; Diukanovic, Ratko; Carroll, Mary; Gratziou, Christina; Smith, Lee A.; Britten, Karen M.; Lee, T. H.; Holgate, Stephen T.

doi:10.1016/0091-6749(91)91568-e

Cited by 45 publications

(68 citation statements)

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“…The primary goal of this and previous studies [11] was to investigate whether differences in VCAM expression could account for the differences in inflammatory cell profile between severe and mild asthmatics [11], and the authors therefore specifically selected patients who represented the two extremes of the disease spectrum. Previous studies have already shown that treatment of mild and moderately severe asthmatics with glucocorticoids is associated with a marked depletion of eosinophils and downregulation of T-lymphocyte activation with no differences in the expression of ICAM-1 and E-selectin [9]. The present study extends previous postmortem observations [5,6] by showing that in living patients with severe asthma increased vascularity is associated with increased numbers of vessels expressing ICAM-1.…”

Section: Discussionsupporting

confidence: 88%

“…However, long-term incubation of endothelial cells with glucocorticoids and TNF-a does not affect ICAM-1 expression [26,27]. These observations are consistent with those made by MONTEFORT et al [9], who demonstrated that both ICAM-1 and E-selectin expression in bronchial biopsies remained unaltered after 6 weeks of treatment with high doses of topical glucocorticoids (2,000 mg . day -1 ).…”

Section: Discussionsupporting

confidence: 83%

“…This is followed by adhesion through the interaction between integrins expressed on leukocytes and intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 expressed on the endothelium. Studies on bronchial biopsy specimens obtained from mild asthmatics have demonstrated constitutive expression of I-CAM-1 and, to a lesser extent, E-selectin on the bronchial microvasculature, which was not significantly different from normal subjects [9,10]. The authors have recently demonstrated an increase in the number of T-cells expressing the activation marker CD25 (interleukin (IL)-2 receptor) in bronchial biopsies from clinically unstable glucocorticoid-dependent asthmatics in comparison to mild asthmatics and normals [11].…”

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confidence: 92%

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Bronchial angiogenesis in severe glucocorticoid-dependent asthma

Vrugt¹,

Wilson²,

Bron³

et al. 2000

Eur Respir J

131

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To examine the role of the bronchial microvasculature and adhesion molecule expression in severe asthma, the authors have performed an immunohistochemical study on bronchial biopsies comparing 15 glucocorticoid-dependent asthmatics, 15 mild asthmatics and eight control subjects.Serially cut glycol methacrylate-embedded sections were stained with monoclonal antibodies identifying the vessel marker EN-4, intercellular adhesion molecule (I-CAM)-1, vascular cell adhesion molecule (VCAM)-1, E-and P-selectin. Sections were also stained for lymphocyte function associated antigen (LFA)-1 and very late antigen (VLA)-4.By comparison with mild asthma and nonasthma, severe asthma was characterized by increased numbers of submucosal vessels (p=0.009) which was associated with increased numbers of vessels expressing ICAM-1 (p=0.005). A highly significant correlation was found between the total number of EN-4+ vessels and the vessels expressing ICAM-1 (r=0.85, p=0.01). In contrast, E-selectin expression was lower in severe as compared with mild asthma (p=0.01) but not different from normal. No differences were found between the three groups in the expression of VCAM-1 and Pselectin nor in numbers of LFA-1+ and VLA-4+ cells.The results of this study support the notion that mucosal neovascularization is an important feature of airways remodelling in severe asthma. This is associated with a relatively higher density of vessels expressing intercellular adhesion molecule-1, although the expression of this adhesion molecule per vessel was not raised.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionsupporting

confidence: 83%

mentioning

confidence: 92%

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Bronchial angiogenesis in severe glucocorticoid-dependent asthma

Vrugt¹,

Wilson²,

Bron³

et al. 2000

Eur Respir J

131

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“…This may be an important mechanism in the regulation of the access of leucocytes to the lung parenchyma during pulmonary immune and inflammatory reactions, including idiopathic pulmonary fibrosis, sarcoidosis, and other interstitial lung diseases. ICAM-1 is also constitutively expressed in human bronchial epithelium [12], and its expression increases after allergen challenge in human asthma, in parallel with an increase in neutrophils, eosinophils, T-cells, and mast cells [13]. In addition, ICAM-1 is known to be the major surface receptor for rhinoviruses, which may produce lung diseases [14].…”

Section: Discussionmentioning

confidence: 99%

ICAM-1 and integrin expression on isolated human alveolar type II pneumocytes

Guzman¹,

Izumi²,

Nagai³

et al. 1994

Eur Respir J

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Adhesion molecules are involved in the recruitment of leucocytes to sites of inflammation. In this study, we determined the expression of several adhesion molecules on isolated human alveolar type II pneumonocytes. Type II pneumocytes were isolated from 10 normal lung specimens, by enzymatic digestion with dispase, followed by metrizamide gradient centrifugation and panning on immunoglobulin G (IgG)-coated plastic dishes. With the freshly isolated type II cells, immunostaining was performed using a sensitive immunoperoxidase slide technique. In all cases, 60-90% of type II cells were positive for intercellular adhesion molecule-1 (ICAM-1) (CD54). A minor portion of type II cells expressed the alpha 4 (CD49d) subunit of the beta 1-integrins, and the alpha-v (CD51) subunit of the vitronectin receptor. CD11a, CD11b, CD11c, CD18, CD49b, and CD49f failed to demonstrate any immunostaining with type II cells. In conclusion, the observation of the expression of ICAM-1 and, to a lesser degree, of some integrin subunits, may indicate that alveolar type II cells participate in local immune and inflammatory responses.

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“…Despite this promising and exciting demonstration, very few studies have been done on this topic in man. As far as asthma is concerned, Montefort et al (44) reported the presence of ICAM-1 on epithelial cells of both asthmatic patients and controls, whereas Campbell et al (13) found ICAM-1 presence on bronchial epithelium of asthmatic subjects in primary culture upon histamine supplementation.…”

Section: Epithelial Cells Adhesion Molecules and Inflammationmentioning

confidence: 99%