title: Cetirizine reduces ICAM-I on epithelial cells during nasal minimal persistent inflammation in asymptomatic children with mite-allergic asthma.
abstract: It has been recently demonstrated that individuals who suffer from mite allergy present mucosal inflammation even when asymptomatic. This situation is characterized by infiltration of inflammatory cells (eosinophils and neutrophils) and by ICAM-I expression on epithelial cells. It has been called 'minimal persistent inflammation' (MPI) for its relationship with natural exposure to allergen, which is continuous in the case of mite allergy. ICAM-I (or CD54) expression on epithelial cells is relevant for several reasons: (a) healthy individuals and patients with pollen allergy out of the pollen season do not express this molecule; (b) ICAM-I is the natural ligand of LFA-1 (an integrin expressed on granulocytes), and (c) ICAM-I is also receptor for rhinoviruses. It is well known that viral infections precede asthmatic attacks; consequently, this correlation is more frequent in cases of mite allergy. Cetirizine is an antiallergic drug that can reduce both inflammatory infiltrate and ICAM-I expression induced by allergen-specific conjunctival challenge. The aim of this study was to evaluate the effect of cetirizine on MPI in 20 children (5-14 years old) with mite allergy. All the children suffered from mild asthma and 9 also had rhinitis (they had been asymptomatic, and thus not treated, for 2 months). The study was double-blind, placebo controlled and randomized and children took Cetirizine or placebo for 15 days. At the beginning and end of the study, nasal scrapings were performed to evaluate inflammatory cell infiltration (eosinophils and neutrophils) and ICAM-I expression on epithelial cells. Cetirizine-treated children showed a significant reduction (or even total absence) of ICAM-I expression on epithelial cells (p less than 0.002) and a reduction trend in inflammatory cell counts compared with placebo. In conclusion, Cetirizine might be envisaged as fruitful for the prolonged treatment of allergic children, including during clinical latency, to prevent possible relapse or rhinovirus infections.
authors.affiliation: First Pediatric Clinic, Institute G. Gaslini, Genoa, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Fasce
authors.forename: G
authors.initials: G
authors.lastname: Ciprandi
authors.forename: C
authors.initials: C
authors.lastname: Pronzato
authors.forename: S
authors.initials: S
authors.lastname: Cozzani
authors.forename: M A
authors.initials: MA
authors.lastname: Tosca
authors.forename: I
authors.initials: I
authors.lastname: Grimaldi
authors.forename: G W
authors.initials: GW
authors.lastname: Canonica
mesh_terms: D000293:Adolescent; D000485:Allergens / Q000276:immunology; D000818:Animals; D039741:Antigens, Dermatophagoides; D001249:Asthma / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology*; D017332:Cetirizine / Q000494:pharmacology*; D002648:Child; D002675:Child, Preschool; D004311:Double-Blind Method; D004848:Epithelium / Q000187:drug effects / Q000473:pathology; D006023:Glycoproteins / Q000276:immunology*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000187:drug effects*; D008925:Mites / Q000276:immunology*; D009297:Nasal Mucosa / Q000187:drug effects* / Q000473:pathology*
chemical_list: D000485:Allergens; D039741:Antigens, Dermatophagoides; D006023:Glycoproteins; D018799:Intercellular Adhesion Molecule-1; D017332:Cetirizine