Circulating intracellular adhesion molecule-1 concentrations following bronchial provocation in atopic asthma.
A house dust bronchial provocation test (BPT) was used to investigate the effect of allergen-induced airway inflammation and airway hyperresponsiveness (AHR) on the level of circulating intracellular adhesion molecule-1 (c-ICAM-1). The concentration of c-ICAM-1 was measured by the sandwich ELISA while the level of eosinophil cationic protein (ECP) in the sputum was determined by RIA. The parameter used for quantification of AHR was the minimum dose of methacholine (Mch) required to produce a fall in respiratory resistance and was expressed as log Dmin. Fourteen subjects with mild atopic asthma participated in this study. Ten patients (dual asthmatic response group; DAR group) developed a late asthmatic response (LAR) following an immediate asthmatic response (IAR). Four subjects (IAR alone group) exhibited only IAR following BPT. In both groups, the mean baseline concentration of c-ICAM-1 did not change 6 h after BPT (from 195.3+/-20.3 to 220.9+/-27.6 and from 215.5+/-23.5 to 231.3+/-30.5 ng/ml, respectively). However, BPT produced a significant increase in the mean concentration of c-ICAM-1 24 h later in the DAR group (257.3+/-41.14 ng/ml, p < 0.05), but not in the IAR alone group (225.5+/-18.1 ng/ml). BPT also increased ECP levels in the sputum from a baseline value 24 h after BPT in the DAR group (from 30.2+/-10.1 to 68.8+/-19.8 ng/ml; p<0.05), but not in the IAR alone group (from 28.1+/-8.3 to 43.3+/-23.7 ng/ml). There was a significant (p<0.05) correlation between c-ICAM-1-concentrations and sputum ECP levels 24 h after BPT in each group. Furthermore an inverse and significant (p<0.05) correlation was found between c-ICAM-1 concentrations and percent changes in log Dmin 24 h after BPT in each group. Our results suggest that increased concentrations of c-ICAM-1 after BPT may reflect the upregulated expression of airway ICAM-1 during allergen-induced airway inflammation. We propose that c-ICAM-1 is a useful marker for allergic inflammation, particularly that of eosinophilic infiltration into the airway, an essential feature of asthma.
Gonokami
Y
Y
First Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan.
Konno
S
S
Kurokawa
M
M
Kawazu
K
K
Ueno
K
K
Tomita
K
K
Ike
M
M
Nyui
M
M
Adachi
M
M
D000280:Administration, Inhalation; D000328:Adult; D000485:Allergens / Q000008:administration & dosage; D001249:Asthma / Q000175:diagnosis / Q000209:etiology / Q000276:immunology*; D016535:Bronchial Hyperreactivity / Q000097:blood / Q000209:etiology / Q000276:immunology*; D001985:Bronchial Provocation Tests; D004391:Dust / Q000009:adverse effects; D004804:Eosinophils / Q000378:metabolism; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000097:blood / Q000209:etiology / Q000276:immunology*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D008297:Male; D013601:T-Lymphocytes / Q000276:immunology
D000485:Allergens; D004391:Dust; D018799:Intercellular Adhesion Molecule-1