Kaempferol suppresses eosionphil infiltration and airway inflammation in airway epithelial cells and in mice with allergic asthma

J Nutr. 2012 Jan;142(1):47-56. doi: 10.3945/jn.111.150748. Epub 2011 Dec 7.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Asthma / immunology
  • Asthma / pathology*
  • Base Sequence
  • Blotting, Western
  • Bronchitis / immunology
  • Bronchitis / pathology
  • Bronchitis / prevention & control*
  • CD18 Antigens / metabolism
  • Cell Line
  • DNA Primers
  • Eosinophils / drug effects*
  • Eosinophils / immunology
  • Eosinophils / metabolism
  • Humans
  • Hypersensitivity / immunology
  • Hypersensitivity / pathology*
  • Intercellular Adhesion Molecule-1 / metabolism
  • Kaempferols / pharmacology*
  • Mice
  • Mice, Inbred BALB C
  • NF-kappa B / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • CD18 Antigens
  • DNA Primers
  • Kaempferols
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • Intercellular Adhesion Molecule-1
  • kaempferol