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Hemin, a heme oxygenase substrate analog, inhibits the cell surface expression of CD11b and CD66b on human neutrophils
Author(s) -
Andersson J. A.,
Egesten A.,
Cardell L. O.
Publication year - 2002
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1034/j.1398-9995.2002.23593.x
Subject(s) - hemin , integrin alpha m , cd63 , heme oxygenase , immunology , inflammation , flow cytometry , immune system , allergic inflammation , chemotaxis , myeloperoxidase , chemistry , microbiology and biotechnology , biology , biochemistry , heme , enzyme , receptor , microrna , microvesicles , gene
Neutrophils are signaled to sites of infection and inflammation by different chemotactic stimuli. In order to reach the airways they have to adhere to, and then migrate through, the endothelium of pulmonary vessels. Carbon monoxide (CO) is a gaseous mediator, endogenously produced in the human airways. Increased CO production has been demonstrated during airway inflammation and CO as well as hemin, a substrate for CO producing enzymes, has been shown to affect neutrophil migration. Our objective was to investigate if the neutrophil cell surface expression of CD11b, CD66b and CD63 was changed during intermittent allergic rhinitis and to establish whether CO could affect the expression of these markers of cellular activation.