Circulating adhesion molecules in asthma.

Montefort, Stephen; Lai, Chingfeng; Kapahi, Pankaj; Leung, Joseph; Lai, K. N.; Chan, Hing‐Yuen; Haskard, Dorian O.; Howarth, PH; Holgate, S. T.

doi:10.1164/ajrccm.149.5.7513593

Cited by 99 publications

(73 citation statements)

References 7 publications

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“…The levels of these factors at the exacerbations caused by URTIs did not differ from those in patients with acute asthma without obvious URTIs. The levels of these factors are consistent with the data as previously described in acute asthma without obvious URTIs (Montefort et al 1994;Yokoyama et al 1995; Niimi et al 1998). These findings, therefore, suggest that virus infection may also produce the factors that induce inflammation and bronchospasm observed in acute asthma caused by other than virus infection.…”

Section: Discussionsupporting

confidence: 91%

“…Levels of sICAM-1 are reported to increase in the serum and sputum of patients with acute bronchial asthma, bronchopulmonary dysplasia, and other inflammatory and immune disorders (Chihara et al 1994;Montefort et al 1994). Likewise, respiratory viruse infections increase ICAM-1 in airway epithelial cells (Terajima et al 1997;Yamaya 2002) and in vascular endothelial cells (Colden-Stanfield et al 1993).…”

Section: Discussionmentioning

confidence: 99%

“…Increased circulating serum levels of IL-6 (Hashimoto et al 1994;Yokoyama et al 1995), soluble intercellular adhesion molecule-1 (sI-CAM-1) (Montefort et al 1994) and ECP (Niimi et al 1998), and concentrations of urine leukotriene E 4 (LTE 4 ) (Oosaki et al 1997) and plasma histamine (Calhoun et al 1991) have been reported in symptomatic acute asthma (Montefort et al 1994;Yokoyama et al 1995;Oosaki et al 1997;Niimi et al 1998), in children with acute respiratory infection (Hashimoto et al 1994), and in experimental RV infection in allergic subjects after antigen bronchoprovocation (Calhoun et al 1991). However, the relationship between the airway narrowing and the increases in these factors has not been studied in patients with asthma exacerbations caused by spontaneously developed upper respiratory tract infections (URTIs).…”

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confidence: 99%

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Inflammatory and Bronchospastic Factors in Asthma Exacerbations Caused by Upper Respiratory Tract Infections

Yasuda

Suzuki

Zayasu

et al. 2005

Tohoku J. Exp. Med.

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It is still uncertain how viral respiratory infections cause acute exacerbations of bronchial asthma, although several mechanisms have been proposed. We studied the relationship between the airway narrowing and the inflammatory and bronchospastic factors in peripheral venous blood and urine, in 30 patients with asthma at the exacerbations caused by upper respiratory tract infections (URTIs). Acute exacerbations caused decreases in peak expiratory flow rate (PEFR) in all 30 patients with asthma. Asthma exacerbations caused the rises in serum levels of interleukin-6, soluble intercellular adhesion molecule-1 and eosinophil cationic protein, concentrations of urinary leukotriene E 4 and plasma histamine, compared with those in patients with asthma at a stable condition and those in 30 control subjects (p < 0.05). The values of PEFR at the exacerbations correlated with the levels of these factors. Treatment with oral glucocorticoids reversed the decreases in PEFR and the increases in these factors. At the onset of URTIs, rhinovirus and influenza type A virus were identified in 13 and 7 patients, respectively. Each of parainfluenza virus, adenovirus, and enterovirus was identified in one patient. These findings suggest that respiratory viral infections may cause acute asthma exacerbations via the production of mediators that induce inflammation and bronchospasm. bronchial asthma; virus infection; interleukin-6; ICAM-1; leukotriene; histamine

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Inflammatory and Bronchospastic Factors in Asthma Exacerbations Caused by Upper Respiratory Tract Infections

Yasuda

Suzuki

Zayasu

et al. 2005

Tohoku J. Exp. Med.

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“…Potential mediators responsible for leukocyte attachment to endothelium include intercellular adhesion molecule-1 (ICAM-1), interleukin-8 (IL-8), and monocyte chemoattractant protein-1 (MCP-1). It has been reported that ICAM-1, a member of the immunoglobulin superfamily, is required for leukocyte migration into inflamed area (3,6,35) and plays an important role in inflammatory disease, including bronchial asthma, lung injury, and ischemic heart disease (18)(19)(20)(21)(22). IL-8, a CXC chemokine that induces the migration and proliferation of endothelial cells and smooth muscle cells, is a potent angiogenic factor that may play a substantial role in atherosclerosis (4,31).…”

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confidence: 99%

Effects of obstructive sleep apnea on circulating ICAM-1, IL-8, and MCP-1

Ohga

Tomita

Wada

et al. 2003

Journal of Applied Physiology

306

180

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structive sleep apnea syndrome (OSAS) is one of the most important risk factors of cardiovascular disorders. In the treatment of OSAS, nasal continuous positive airway pressure (nCPAP) has been widely used and found to be effective. In the present study, we hypothesized that the hypoxic stress caused by obstructive sleep apnea would increase circulating intercellular adhesion molecule-1 (ICAM-1), interleukin-8 (IL-8), and monocyte chemoattractant protein-1 (MCP-1) in untreated OSAS patients compared with an age-matched control group. In addition, we hypothesized that nCPAP may decrease OSAS-induced hypoxic stress and mediators. To examine these hypotheses, we measured circulating ICAM-1 and IL-8 before and after nCPAP therapy in OSAS patients. We observed that nCPAP decreased apnea, desaturation, and the circulating ICAM-1 and IL-8 levels in OSAS patients. The circulating levels of ICAM-1, IL-8, and MCP-1 in untreated OSAS patients were significantly greater than those in the controls. These observations suggest that nCPAP therapy could reduce OSAS-induced hypoxia and generation of inflammatory mediators. Treatment of OSAS using nCPAP can be, therefore, a potential approach to decrease risk of the progression of OSAS-associated disorders. cytokines; cardiovascular disorders; ischemic heart disease; desaturation magnitude; hypoxic stress; intracellular adhesion molecule-1; monocyte chemoattractant protein-1; interleukin-8

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“…Several studies have demonstrated that CD11/ CD18, E-selectin and ICAM-1 are important determinants in neutrophil trafficking [29±34]. Up-regulation of circulating E-selectin and ICAM-1 is found in the airways of patients with asthma and cystic fibrosis [15,16], where marked airway infiltration by eosinophils or neutrophils occurs. Antibodies against E-selectin and ICAM-1 block neutrophil extravasation in rat lungs [33], and inhibit neutrophil trafficking into the inflamed lungs of a rabbit [34].…”

Section: Discussionmentioning

confidence: 99%

Up-regulation of circulating adhesionmolecules in bronchiectasis

Zheng

Tipoe²,

Lam³

et al. 2000

Eur Respir J

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Adhesion molecules are expressed on the surface of endothelial cells and leukocytes and are responsible for mediating the migration of intravascular leukocytes into inflamed tissue. Intensive recruitment of neutrophils into the airways occurs in bronchiectasis, although little is known about the role of adhesion molecules in this process.The authors, therefore, determined serum levels of E-selectin, intercellular adhesion molecule (ICAM)-1 and vascular adhesion molecule (VCAM)-l in stable bronchiectasis patients (n=37) and healthy control subjects (n=17), and evaluated their relationship with clinical markers of disease severity in bronchiectasis.Serum levels of E-selectin, ICAM-1 and VCAM-1 in bronchiectasis patients were significantly higher than those in control subjects (p=0.02, <0.0001 and 0.0002 respectively). Both E-selectin and ICAM-1 levels were inversely related to forced expiratory volume in one second (FEV1)% predicted (r=-0.57, p<0.001; and r=-0.53, p=0.001 respectively), and FVC% predicted (r=-0.52, p=0.002; and r=-0.46, p=0.005). This was not the case for VCAM-1 levels. There was a correlation between serum ICAM-1 levels and 24 h sputum volume (r=0.34, p= 0.04). Serum E-selectin and ICAM-1, but not VCAM-1, levels showed correlation with the number of lung lobes affected by bronchiectasis (r=0.35, p=0.04 and r=0.34, p=0.04 respectively).These original observations strongly suggest that E-selectin, intercellular adhesion molecule-1 and Vascular adhesion molecule-1 could play a significant role in the pathogenesis of bronchiectasis. Eur Respir J 2000; 16: 691±696.

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Circulating adhesion molecules in asthma.

Cited by 99 publications

References 7 publications

Inflammatory and Bronchospastic Factors in Asthma Exacerbations Caused by Upper Respiratory Tract Infections

Inflammatory and Bronchospastic Factors in Asthma Exacerbations Caused by Upper Respiratory Tract Infections

Effects of obstructive sleep apnea on circulating ICAM-1, IL-8, and MCP-1

Up-regulation of circulating adhesionmolecules in bronchiectasis

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