Epigallocatechin-3-gallate reduces airway inflammation in mice through binding to proinflammatory chemokines and inhibiting inflammatory cell recruitment.
J Immunol
; 186(6): 3693-700, 2011 Mar 15.
Article
en En
| MEDLINE
| ID: mdl-21307292
ABSTRACT
One major activity of chemokines is the recruitment of immune cells to sites of infection and inflammation. CD4(+) Th1 cells play critical roles in host defense against pathogens and in the pathogenesis of many immune-mediated diseases. It was reported that epigallocatechin-3-gallate (EGCG) exhibits anti-inflammatory properties, but the mechanisms have not been completely defined. In this study, we found that EGCG markedly decreased recruitment of murine OVA-specific Th1 cells and other inflammatory cells into the airways in a Th1 adoptive-transfer mouse model. In vitro analysis revealed that EGCG inhibited CXCR3 ligand-driven chemotaxis of murine and human cells. Surface plasmon resonance studies revealed that EGCG bound directly to chemokines CXCL9, CXCL10, and CXCL11. These results indicated that one anti-inflammatory mechanism of EGCG is binding of proinflammatory chemokines and limiting their biological activities. These findings support further development of EGCG as a potent therapeutic for inflammatory diseases.
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Inhibición de Migración Celular
/
Catequina
/
Mediadores de Inflamación
/
Quimiocinas
/
Pulmón
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
J Immunol
Año:
2011
Tipo del documento:
Article
País de afiliación:
Estados Unidos