Oral flavonoids delay recovery from experimental autoimmune encephalomyelitis in SJL mice.
Flavonoids are food components that appear to have potential beneficial health effects. There is a range of in vitro studies supporting the anti-oxidant and anti-inflammatory properties of flavonoids. Previously, we demonstrated that in vitro flavonoids, including luteolin and apigenin, inhibit proliferation and IFN-gamma production by murine and human autoimmune T cells. In the present study, we examined the effects of oral flavonoids as well as of curcumin on autoimmune T cell reactivity in mice and on the course of experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. Continuous oral administration of flavonoids significantly affected antigen-specific proliferation and IFN-gamma production by lymph node-derived T cells following immunization with an EAE-inducing peptide. Both luteolin and apigenin suppress proliferative responses as they did in vitro, whereas IFN-gamma production on the other hand was enhanced. Other flavonoids exerted differential effects on proliferation and IFN-gamma production. The effects of flavonoids and curcumin on EAE were assessed using either passive transfer of autoimmune T cells or active disease induction. In passive EAE, flavonoids led to delayed recovery of clinical symptoms rather than to any reduction in disease. In active EAE, the effects were less pronounced but also, in this case, the flavonoid hesperitin delayed recovery. Oral curcumin had overall mild but beneficial effects. Our results indicate that oral flavonoids fail to beneficially influence the course of EAE in mice but, instead, suppress recovery from acute inflammatory damage.
Verbeek
Richard
R
Business Unit Biomedical Research, TNO Quality of Life, P.O. Box 2215, 2301 CE Leiden, The Netherlands.
van Tol
Eric A F
EA
van Noort
Johannes M
JM
D000284:Administration, Oral; D000818:Animals; D002478:Cells, Cultured; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D005419:Flavonoids / Q000008:administration & dosage* / Q000009:adverse effects; D044948:Flavonols; D006027:Glycosides / Q000008:administration & dosage; D006131:Growth Inhibitors / Q000008:administration & dosage; D006133:Growth Substances / Q000008:administration & dosage; D047311:Luteolin / Q000008:administration & dosage; D051379:Mice; D008815:Mice, Inbred Strains; D011794:Quercetin / Q000008:administration & dosage; D020127:Recovery of Function / Q000187:drug effects* / Q000502:physiology; D013601:T-Lymphocytes / Q000166:cytology / Q000187:drug effects / Q000473:pathology; D047309:Flavones
D005419:Flavonoids; D044948:Flavonols; D006027:Glycosides; D006131:Growth Inhibitors; D006133:Growth Substances; D047311:Luteolin; D011794:Quercetin; C120120:alhagidin; C008548:morin; D047309:Flavones; C017875:fisetin