title: Eotaxin expression and eosinophilic inflammation in asthma.
abstract: Asthma is a chronic inflammatory disease of the airways characterized by a marked infiltration of eosinophils in the bronchial mucosa, and the mechanisms that cause the selective recruitment of these cells are areas of active investigation. In this study, we found increased expression of the eosinophil chemoattractant eotaxin in bronchial mucosa of asthmatic patients. The increase in number of cells expressing eotaxin mRNA correlated with the number of eosinophils in the bronchial tissue and with two major clinical and functional indices of disease severity, suggesting that eotaxin is involved in the recruitment of eosinophils and in eosinophil-induced tissue damage in asthma. Cell sources of eotaxin were bronchial epithelial cells, T lymphocytes, macrophages and eosinophils themselves. The use of drugs that interfere with eotaxin synthesis and function may represent a more specific approach in asthma treatment.
authors.affiliation: Institute of Experimental Medicine, Milan, Italy.
authors.forename: S
authors.initials: S
authors.lastname: Mattoli
authors.forename: M A
authors.initials: MA
authors.lastname: Stacey
authors.forename: G
authors.initials: G
authors.lastname: Sun
authors.forename: A
authors.initials: A
authors.lastname: Bellini
authors.forename: M
authors.initials: M
authors.lastname: Marini
mesh_terms: D001249:Asthma / Q000503:physiopathology*; D001980:Bronchi / Q000378:metabolism*; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D004804:Eosinophils / Q000502:physiology*; D015870:Gene Expression; D006801:Humans; D017403:In Situ Hybridization; D007249:Inflammation / Q000503:physiopathology*; D009092:Mucous Membrane / Q000378:metabolism; D014158:Transcription, Genetic
chemical_list: C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines