Cell infiltration, ICAM-1 expression, and eosinophil chemotactic activity in asthmatic sputum.

Louis, Renaud; Shute, Janis K.; Biagi, S.; Stanciu, Luminita A.; Marrelli, F.; Tenor, H.; Hidi, Rabiâ; Djukanović, Ratko

doi:10.1164/ajrccm.155.2.9032180

Cited by 96 publications

(116 citation statements)

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“…ICAM-1 is expressed on a minority of blood T-cells, but is upregulated several-fold on T-cells in the airways lumen with further upregulation being seen in inflammatory conditions such as asthma [13].…”

Section: Expression Of Icam-1 On T-cells During Activation and Homingmentioning

confidence: 99%

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

Stanciu¹,

Djukanović²

1998

Eur Respir J

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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.

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Section: Expression Of Icam-1 On T-cells During Activation and Homingmentioning

confidence: 99%

“…A low percentage of circulating blood T-cells expresses ICAM-1 in contrast to the high levels of LFA-1 expression [13]. Mitogen and antigen-specific stimulation [55], cytokines (IFN-γ, IL-1β, IL-2 and TNF-α) [11] and viruses [56,57] may all cause up-regulation of ICAM-1 on the T-cell surface.…”

Section: Modulation Of Icam-1 On T-cellsmentioning

confidence: 99%

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

Stanciu¹,

Djukanović²

1998

Eur Respir J

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“…Cell viability with trypan blue and a total cell count is then determined in a haemocytometer and cytospins are prepared and stained for a 400-500 differential cell count. The cells can also be examined by immunocytochemistry [76][77][78][79][80], in situ hybridisation [81] or flow cytometry [82][83][84]. The filtrate can be spun to obtain the fluid phase, which is stored at -70uC for future measurements [44,45].…”

Section: Sputum Inductionmentioning

confidence: 99%

Airway inflammation in COPD: physiological outcome measures and induced sputum

Crapo

Jensen²,

Hargreave³

2003

European Respiratory Journal

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Chronic obstructive pulmonary disease (COPD) is a result of airway inflammation, and the best predictor of COPD is the early detection of airflow limitation by spirometry. The Global Initiative for Obstructive Lung Disease Workshop Report defines airflow limitation using simple spirometric indices. Available guidelines categorise the severity of COPD using forced expiratory volume in one second (FEV1) and forced vital capacity (FVC), with symptoms playing a minor role in the assessment.Current standards define COPD by progressive loss of FEV1, and thus longitudinal decline in FEV1 will be the primary outcome variable for intervention studies aimed at preventing or reducing the loss of pulmonary function. There is evidence, however, that the variable FEV1/FVC and FEV1 are often not measured properly in all settings.This article will discuss the roles of physiological measurements in diagnosing COPD and physiological outcome measures for COPD. It does not formally compare physiological measures with other outcome measures, such as symptoms or quality of life. Additionally, improved treatment of established disease requires a better understanding of the inflammatory process and its clinical effects and treatment.The inflammatory process, and how drugs affect it, can be studied noninvasively or relatively noninvasively by using refined methods of examining spontaneous or induced sputum. Enhanced understanding of the use of induced sputum will assist in predicting patients9 responses to short-and long-term inhaled corticosteroid treatment, and the methods of sputum examination need to be simplified so that they can be applied more easily to clinical practice. Eur Respir J 2003; 21: Suppl. 41, 19s- Chronic obstructive pulmonary disease (COPD) is defined by the Global Initiative for Obstructive Lung Disease (GOLD) as a "disease state characterised by airflow limitation that is not fully reversible. …The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases" [1]. The absence of reversibility tends to exclude asthma by definition, although asthma can coexist with COPD. Methods of assessing airflow limitation: current recommendations and their limitationsAvailable guidelines categorise the severity of COPD primarily by using forced expiratory volume in one second (FEV1), whereas symptoms play a minor role in the assessment [1][2][3][4][5]. This tight link between FEV1 and COPD reflects the fact that spirometry is the standard for defining the presence of airway obstruction and the progressive loss of FEV1, the physiological variable that characterises COPD severity and predicts its mortality. Spirometry has become the standard, in part, because good quality and inexpensive tests are widely available.The GOLD Workshop Report explicitly defines airflow limitation using simple spirometric indices. Specifically, airflow limitation is defined as an FEV1/forced vital capacity (FVC)v70% and a postbronchodilator FEV1v80% of predict...

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“…The whole collected sputum was processed using DTT (dithiotreitol, Sigma) 7 mM for 30 min at room temperature and subsequently centrifuged for 10 min (400g) as previously described (16). Total and squamous cell counts were performed on a manual hemocytometer and samples with percentage squamous cell count >30% discarded.…”

Section: Sputum Induction and Processingmentioning

confidence: 99%

Increased Response of Blood Eosinophils to Various Chemotactic Agents in Quiescent Crohn Disease

Denis¹,

Louis²,

Malaise³

et al. 2001

Scandinavian Journal of Gastroenterology

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Background: The number of eosinophils is increased in the mucosae of the digestive and the respiratory tracts in Crohn disease, even clinically quiescent. The mechanisms underlying this panmucosal eosinophilia are unknown. Methods: The response of blood eosinophils to various chemotactic agents was assessed in 15 patients with clinically quiescent Crohn disease. The results were compared with 15 healthy controls. After purification, eosinophils were placed in Boyden microchambers and the chemotactic effect of PAF (10 -7 M), RANTES (50ng/ml), IL-5 (0-20ng/ml), IL-8 (0-50ng/ml), Eotaxin (0-50 ng/ml) was evaluated. The number of eosinophils in induced sputum of these Crohn disease patients and controls was also assessed and the correlation between chemotaxis and eosinophil count in induced sputum was studied.

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Cell infiltration, ICAM-1 expression, and eosinophil chemotactic activity in asthmatic sputum.

Cited by 96 publications

References 0 publications

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

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

Airway inflammation in COPD: physiological outcome measures and induced sputum

Increased Response of Blood Eosinophils to Various Chemotactic Agents in Quiescent Crohn Disease

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