title: Epigallocatechin-3-gallate reduces airway inflammation in mice through binding to proinflammatory chemokines and inhibiting inflammatory cell recruitment.
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.
authors.affiliation: Department of Infectious Diseases and Microbiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15261, USA.
authors.forename: Shulin
authors.initials: S
authors.lastname: Qin
authors.forename: John F
authors.initials: JF
authors.lastname: Alcorn
authors.forename: Jodi K
authors.initials: JK
authors.lastname: Craigo
authors.forename: Charis
authors.initials: C
authors.lastname: Tjoeng
authors.forename: Patrick M
authors.initials: PM
authors.lastname: Tarwater
authors.forename: Jay K
authors.initials: JK
authors.lastname: Kolls
authors.forename: Todd A
authors.initials: TA
authors.lastname: Reinhart
mesh_terms: D000818:Animals; D001665:Binding Sites / Q000276:immunology; D002392:Catechin / Q000031:analogs & derivatives* / Q000378:metabolism / Q000502:physiology; D002464:Cell Migration Inhibition / Q000276:immunology*; D002478:Cells, Cultured; D054357:Chemokine CXCL10 / Q000037:antagonists & inhibitors / Q000378:metabolism; D054371:Chemokine CXCL11 / Q000037:antagonists & inhibitors / Q000378:metabolism; D054370:Chemokine CXCL9 / Q000037:antagonists & inhibitors / Q000378:metabolism; D018925:Chemokines / Q000037:antagonists & inhibitors / Q000378:metabolism*; D004195:Disease Models, Animal; D018836:Inflammation Mediators / Q000378:metabolism / Q000502:physiology*; D008168:Lung / Q000276:immunology* / Q000378:metabolism / Q000473:pathology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D016513:Mice, SCID; D008822:Mice, Transgenic
chemical_list: D054357:Chemokine CXCL10; D054371:Chemokine CXCL11; D054370:Chemokine CXCL9; D018925:Chemokines; C485433:Cxcl10 protein, mouse; C515203:Cxcl11 protein, mouse; C485969:Cxcl9 protein, mouse; D018836:Inflammation Mediators; D002392:Catechin; C045651:epigallocatechin gallate