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PMID: 9240429 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Eotaxin expression and eosinophilic inflammation in asthma.

Biochemical and biophysical research communications ·Vol. 236 ·No. 2 ·1997-07-18 ·Pages 299-301

Mattoli S, Stacey MA, Sun G, Bellini A, Marini M

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.

MeSH Terms
Asthma/physiopathology Bronchi/metabolism Chemokine CCL11 Chemokines, CC Cytokines/genetics,metabolism Eosinophils/physiology Gene Expression Humans In Situ Hybridization Inflammation/physiopathology Mucous Membrane/metabolism Transcription, Genetic
Chemicals
CCL11 protein, human Chemokine CCL11 Chemokines, CC Cytokines
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Mattoli S
Institute of Experimental Medicine, Milan, Italy.
Stacey M A
Sun G
Bellini A
Marini M
Article Info
Journal
Biochemical and biophysical research communications
Abbr.
Biochem Biophys Res Commun
ISSN
0006-291X
Published
1997-07-18
Pages
299-301
Language
English
Region
United States
NLM ID
0372516
Subset
IM
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