期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 10, 期 2, 页码 183-192出版社
ELSEVIER
DOI: 10.1016/j.intimp.2009.10.014
关键词
Quercetin; Basophil activation; CD63; CD203c; Flavonoid; Hormesis; Allergy; Inflammation; Priming
资金
- Ministry of Education, University and Research
- Boiron Laboratoires s.r.l., Milan
Background: Flavonoids, such as quercetin, were reported to inhibit histamine release and cytokine production by basophils, but there is no evidence describing their action on membrane markers and intracellular biochemical pathways. Objective: The aim of the study was to examine the effect of several quercetin doses on an in vitro human basophil activation system that evaluates up-regulation of membrane markers in response to agonists. Methods: Leukocyte buffy coats from K-2-EDTA anti-coagulated blood were treated with different concentrations of quercetin and triggered with anti-IgE (allergy model) and with N-formyl-Met-Leu-Phe (fMLP) (inflammation model). Basophils were captured as CD123(bright)/HLA-DRnon-expressing cells in a flow cytometry analysis and fluorescence values of CD63-FITC, CD203c-PE and CD123-PECy5 were used to produce dose response curves. Results: Quercetin at a dose of 10 mu g/ml strongly inhibited CD63 and CD203c membrane up-regulation triggered by both agonists, but it neither affected cell viability nor changed the expression of the phenotypic marker CD123. The anti-IgE model appeared highly sensitive to the effect of quercetin: a dose as low as 0.01 mu g/ml was able to significantly decrease CD63 and CD203c membrane expression. In the fMLP model the dose response was different: quercetin doses from 0.01 to 0.1 mu g/ml significantly increased up-regulation of membrane markers, achieving the highest effect with CD63. Conclusion: Very low doses of quercetin, within the pharmacological range, inhibit IgE-mediated membrane marker's up-regulation but prime the response to the chemotactic peptide fMLP; this stimulus specificity may have implications on the possible therapeutic action of the flavonoid in different pathologies. (C) 2009 Elsevier B.V. All rights reserved.
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