Allergy.  1995 Sep;15(3):330-341.

Changes of soluble ICAM- 1 levels in serum and bronchoalveolar lavage fluid from patients with atopic bronchial asthma after allergen challenge

Abstract

Leukocyteendothelial adhesion molecules are involved in the initial state of the recruit ment and migration of inflammatory leukocytes from the circulation to sites of inflammation. In allergic inflammation, administ-ration of anti-ICAM-1 monoclonal antibodies into monkeys resulted both in reduced eosinophil infiltration into the lung and in reduced airway hyperresponsiveness, and upregulation of ICAM-1 expression was observed on the endothelium, the bronchial epithelium, and eosinophils, suggesting an important role for ICAM-1 in the pathogenesis of bronchial asthma. To our knowledge, there has been few previous reports concerning solublelCAM-1 (sICAM-l) in patients with atopic bronchial asthma after allergen challenge. If the levels of sICAM-1 vary between bronchial asthma patients and normal controls, this variance would be very useful to assess the state of this disease. Therefore, we attempted to measure the levels of sICAM-1 from 17patients with atopic bronchial asthma. sICAM-1 levels in sera from patients with bronchial asthma were measured at 8 hour after allergen challenge with house dust mite, and prechallenge periods. sICAM-1 levels in BAL fluids were also measured at 30min and 8hour after allergen challenge. sICAM-1 levels in sera from bronchial asthma in prechallenge conditions were higher than in normal control subjects, and sICAM-1 levels in sera from bronchial asthma patients in 8hour after allergen challenge were higher than those in sera obtained during prechallenge periods. sICAM- 1 levels in BAL fluids from bronchial asthma patients in 8hour after allergen challenge were significantly higher than in 30min after allergen challenge. These results suggest that higher levels of sICAM-1 in sera and BAL fluids reflect the upregulation of ICAM-1 expression in allergic bronchial asthma and it may take a role in the pathogenesis of atopic bronchial asthma.


MeSH Terms

Antibodies, Monoclonal
Asthma*
Bronchoalveolar Lavage Fluid*
Bronchoalveolar Lavage*
Endothelium
Eosinophils
Epithelium
Haplorhini
Humans
Inflammation
Intercellular Adhesion Molecule-1
Leukocytes
Lung
Pyroglyphidae
Up-Regulation
Antibodies, Monoclonal
Intercellular Adhesion Molecule-1
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