title: (-)-Epigallocatechin-3-gallate inhibits CC chemokine ligand 11 production in human gingival fibroblasts.
abstract: BACKGROUND
  CC chemokine ligand 11 (CCL11) is related to Th2 cells migration via CC chemokine receptor 3 (CCR3). Th2 cells are involved in the etiology of periodontal disease. However, how the infiltration of Th2 cells is controlled in periodontally diseased tissues is unknown. (-)-Epigallocatechin gallate (EGCG), the major catechin in green tea, has multiple beneficial effects, but the effects of EGCG on CCL11 production are uncertain. In this study, we investigated whether cytokines could induce CCL11 production in human gingival fibroblasts (HGFs). Moreover, we examined the effects of EGCG on CCL11 production in HGFs.
  
  
  RESULTS
  ELISA analysis disclosed that interleukin (IL)-4 synergistically enhanced CCL11 production in IL-1β or tumor necrosis factor (TNF)-α-stimulated HGFs. EGCG prevented IL-1β/ IL-4 or TNF-α/IL-4-mediated CCL11 production in a concentration dependent manner. CCL11 production in HGFs was positively regulated by p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), and c-Jun N terminal kinase (JNK). Western blot analysis revealed that EGCG treatment prevented IL-1β/IL-4 or TNF-α/IL-4-induced ERK and JNK activation in HGFs.
  
  
  CONCLUSIONS
  These data provide that CCL11 production in HGFs could be associated with Th2 cells infiltration in periodontal lesions. Moreover, EGCG is useful for periodontitis treatment to inhibit CCL11 production.
authors.affiliation: Department of Conservative Dentistry and Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Tokushima, Japan. hosokawa@dent.tokushima-u.ac.jp
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Hosokawa
authors.forename: Ikuko
authors.initials: I
authors.lastname: Hosokawa
authors.forename: Satoru
authors.initials: S
authors.lastname: Shindo
authors.forename: Kazumi
authors.initials: K
authors.lastname: Ozaki
authors.forename: Takashi
authors.initials: T
authors.lastname: Matsuo
mesh_terms: D000873:Anthracenes / Q000494:pharmacology; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D002478:Cells, Cultured; D054413:Chemokine CCL11 / Q000378:metabolism*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism; D005347:Fibroblasts / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D005419:Flavonoids / Q000494:pharmacology; D005881:Gingiva / Q000166:cytology*; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D053583:Interleukin-1beta / Q000494:pharmacology; D015847:Interleukin-4 / Q000494:pharmacology*; D048031:JNK Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism; D010766:Phosphorylation; D011725:Pyridines / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects; D018418:Th2 Cells / Q000166:cytology / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D000873:Anthracenes; C515456:CCL11 protein, human; D054413:Chemokine CCL11; D005419:Flavonoids; D007093:Imidazoles; D053583:Interleukin-1beta; D011725:Pyridines; D014409:Tumor Necrosis Factor-alpha; C432165:pyrazolanthrone; D015847:Interleukin-4; D002392:Catechin; C045651:epigallocatechin gallate; D048049:Extracellular Signal-Regulated MAP Kinases; D048031:JNK Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; C093642:SB 203580; C093973:2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one