Abstract
Allergen-specific challenge was first shown to induce ICAM-1 expression on epithelial cells (ECs) of conjunctiva in allergic patients. The data have also been confirmed in the nose. We then checked for the presence of ICAM-1 consequent to natural exposure to allergens. For both conjunctivitis and rhinitis due to pollen we confirmed, during the pollen season, the presence of ICAM-1 on ECs. We demonstrated the endogenous source of ICAM-1 by in situ hybridization both in vitro and in vivo. ICAM-1 could be an activation marker on ECs, or could, enhanced EC susceptibility to bind offending cells such as eosinophils (LFA-1+). ICAM-1 is also a receptor for the vast majority of rhinoviruses, which are known to provoke, mainly in children, asthma attacks. Since we found that mite allergens can induce ICAM-1 on ECs, even during clinical latency, allergy may be considered as a primary event leading to asthma (through rhinovirus infection) and non-specific hyperreactivity.
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