Open AccessQuercetin Induces Apoptosis of Trypanosoma brucei gambiense and Decreases the Proinflammatory Response of Human Macrophages
Author(s) -
Maria Mamani-Matsuda,
Jérôme Rambert,
Denis Malvy,
Hélène Lejoly-Boisseau,
Sylvie Daulouède,
Denis Thiolat,
Sara Coves,
Pierrette Courtois,
Philippe Vincendeau,
M. Djavad Mossalayi
Publication year - 2004
Publication title -
antimicrobial agents and chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.07
H-Index - 259
eISSN - 1070-6283
pISSN - 0066-4804
DOI - 10.1128/aac.48.3.924-929.2004
Subject(s) - quercetin , proinflammatory cytokine , apoptosis , trypanosoma brucei , nitric oxide , tumor necrosis factor alpha , annexin , biology , flavonoid , programmed cell death , cytotoxicity , microbiology and biotechnology , antimicrobial , immunology , pharmacology , inflammation , biochemistry , in vitro , antioxidant , gene , endocrinology
In addition to parasite spread, the severity of disease observed in cases of human African trypanosomiasis (HAT), or sleeping sickness, is associated with increased levels of inflammatory mediators, including tumor necrosis factor (TNF)-alpha and nitric oxide derivatives. In the present study, quercetin (3,3',4',5,7-pentahydroxyflavone), a potent immunomodulating flavonoid, was shown to directly induce the death of Trypanosoma brucei gambiense, the causative agent of HAT, without affecting normal human cell viability. Quercetin directly promoted T. b. gambiense death by apoptosis as shown by Annexin V binding. In addition to microbicidal activity, quercetin induced dose-dependent decreases in the levels of TNF-alpha and nitric oxide produced by activated human macrophages. These results highlight the potential use of quercetin as an antimicrobial and anti-inflammatory agent for the treatment of African trypanomiasis.