Elevated levels of soluble ICAM‐1 in sera from patients with bronchial asthma

Hashimoto, Shigeo; Imai, Kohzoh; Kobayashi, T; Amemiya, E.; Takahashi, Yuwa; Tomita, Yasuyuki; Iwatal, T.; Suguro, Hisashi; Yamaguchi, Masaru; Yachi, Akira; Horie, Takashi

doi:10.1111/j.1398-9995.1993.tb02408.x

Cited by 45 publications

(34 citation statements)

References 7 publications

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“…We also found highly significant correlations between serum sICAM–1 levels and the physiological parameters (RR, PEFR, O 2 % and PaCO 2 ) on which our assessment of the severity of asthma exacerbation was based. Hashimoto et al [15]in their study conducted on adult asthmatics found that serum sICAM–1 levels in sera obtained during bronchial asthma attacks were higher than those in sera obtained from stable asthmatic or normal subjects, which is similar to our observations. Furthermore, they found that serum sICAM–1 levels in atopic asthmatic patients in stable conditions were higher than in normal controls.…”

Section: Discussionsupporting

confidence: 82%

“…In contrast to our results and the aforementioned studies [14, 15, 20], Ceyhan et al [22]suggested that serum sICAM–1 levels are not increased in asthmatic patients as compared with controls and do not correlate with clinical asthma severity. These differences may be explained by multiple factors, notably the very small number of patients enrolled in their study (15 asthmatic patients and 5 controls), adults versus children, and their asthmatic patients had a relatively stable asthma.…”

Section: Discussioncontrasting

confidence: 56%

“…No such marker has yet been found for asthma. Although the reports on the level of serum sICAM–1 in healthy individuals and in inflammatory diseases (especially asthma) in adults are plethoric [14, 15, 20], those in children are scanty. In this study, a soluble circulating form of the usually membrane–bound sICAM–1 was identified and measured in the sera of all healthy control children without a significant difference between boys and girls.…”

Section: Discussionmentioning

confidence: 99%

“…The structural and functional characteristics of sICAM–1 suggest that it chould serve as a fluid–phase regulator of the adhesive interaction [12, 13, 14]. A soluble form of ICAM–1 (sICAM–1) was found in increased levels in patients with inflammatory, immune or malignant diseases [12, 14, 15, 16]. However, most published researches have been carried out on adults.…”

Section: Introductionmentioning

confidence: 99%

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Soluble Intercellular Adhesion Molecule–1 in Sera of Children with Bronchial Asthma Exacerbation

El-Sawy

Badr-El-Din²,

El-Azzouni³

et al. 1999

Int Arch Allergy Immunol

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Previous studies have suggested that intercellular adhesion molecule–1 (ICAM–1; CD54) may be involved in the pathogenesis of asthma. In addition, a soluble form of intercellular adhesion molecule–1 (sICAM–1) has been detected in increased concentrations in the sera from adult patients with certain inflammatory, immune, or malignant diseases. To determine whether bronchial asthma exacerbation in children is associated with increased levels of serum sICAM–1 and to investigate the effect of the severity of exacerbation on these levels, the concentrations of sICAM–1 were measured in sera of 20 healthy control children and 45 asthmatic children (15 with mild, 15 with moderate, and 15 with severe asthma exacerbation) using an immunoenzymatic assay. Assessment of the severity of asthma exacerbation was based on clinical and physiological parameters. The mean (± SD) level of serum sICAM–1 for asthmatic children (390.0±108.3 ng/ml) was significantly higher than that for healthy (193.2±33.95 ng/ml; p = 0.000). We have also found a differential rise of serum sICAM–1 level which correlates well with the severity of asthma exacerbation. The elevated concentrations of serum sICAM–1 in acute bronchial asthma may reflect the extensive inflammatory response occurring in the airways during acute exacerbation of the disease with airway obstruction. The results of this study suggest that serum sICAM–1 is a promising serological marker of the severity of inflammation in bronchial asthma in children and it would not only facilitate staging of inflammation but also allow the monitoring of therapy and intervention.

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Section: Discussionsupporting

confidence: 82%

Section: Discussioncontrasting

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Soluble Intercellular Adhesion Molecule–1 in Sera of Children with Bronchial Asthma Exacerbation

El-Sawy

Badr-El-Din²,

El-Azzouni³

et al. 1999

Int Arch Allergy Immunol

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“…Levels of serum sICAM-1 and soluble E-selectin (sE-selectin) are higher in stable asthmatics as compared with controls, and are further increased in acute asthma [87][88][89]. A rise in sICAM-1 occurs both in the serum and BAL of atopic asthmatics 18 h after allergen challenge [90].…”

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

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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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