title: Kaempferol suppresses eosionphil infiltration and airway inflammation in airway epithelial cells and in mice with allergic asthma.
abstract: The airway epithelium is thought to play an important role in the pathogenesis of asthma. Airway epithelial activation may contribute to inflammatory and airway-remodeling events characteristic of asthma. Kaempferol, a flavonoid with antioxidative and antitumor properties, has been studied as an antiinflammatory agent. However, little is known regarding its effects on allergic asthma. Human airway epithelial BEAS-2B cells and eosinophils were used to investigate the effects of kaempferol on endotoxin- or cytokine-associated airway inflammation. Kaempferol, nontoxic at 1-20 μmol/L, suppressed LPS-induced eotaxin-1 protein expression that may be mediated, likely via Janus kinase 2 (JAK2) JAK2 signaling. Additionally, 1-20 μmol/L kaempferol dose-dependently attenuated TNFα-induced expression of epithelial intracellular cell adhesion molecule-1 and eosinophil integrin β2, thus encumbering the eosinophil-airway epithelium interaction. Kaempferol blunted TNFα-induced airway inflammation by attenuating monocyte chemoattractant protein-1 transcription, possibly by disturbing NF-κB signaling. This study further investigated antiallergic activity of kaempferol in BALB/c mice sensitized with ovalbumin (OVA) and challenged with a single dose of OVA. Oral administration of kaempferol attenuated OVA challenge-elevated expression of eotaxin-1 and eosinophil major basic protein via the blockade of NF-κB transactivation, thereby blunting eosinophil accumulation in airway and lung tissue. Therefore, dietary kaempferol is effective in ameliorating allergic and inflammatory airway diseases through disturbing NF-κB signaling.
authors.affiliation: Department of Food and Nutrition, Hallym University, Chuncheon, Korea.
authors.forename: Ju-Hyun
authors.initials: JH
authors.lastname: Gong
authors.forename: Daekeun
authors.initials: D
authors.lastname: Shin
authors.forename: Seon-Young
authors.initials: SY
authors.lastname: Han
authors.forename: Jung-Lye
authors.initials: JL
authors.lastname: Kim
authors.forename: Young-Hee
authors.initials: YH
authors.lastname: Kang
mesh_terms: D000818:Animals; D001249:Asthma / Q000276:immunology / Q000473:pathology*; D001483:Base Sequence; D015153:Blotting, Western; D001991:Bronchitis / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D018821:CD18 Antigens / Q000378:metabolism; D002460:Cell Line; D017931:DNA Primers; D004804:Eosinophils / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology / Q000473:pathology*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D044949:Kaempferols / Q000494:pharmacology*; D051379:Mice; D008807:Mice, Inbred BALB C; D016328:NF-kappa B / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D018821:CD18 Antigens; D017931:DNA Primers; D044949:Kaempferols; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; C006552:kaempferol