The non-proteolytic house dust mite allergen Der p 2 induce NF-kappaB and MAPK dependent activation of bronchial epithelial cells

Clin Exp Allergy. 2009 Aug;39(8):1199-208. doi: 10.1111/j.1365-2222.2009.03284.x. Epub 2009 May 26.

Abstract

Background: House dust mites (HDM) are well-known as a source of indoor aeroallergens and for causing allergic airway diseases. Some proteolytic HDM allergens are known to activate respiratory epithelial cells to produce pro-inflammatory mediators, while there is limited knowledge regarding such activity among non-proteolytic HDM allergens.

Objective: To investigate whether Der p 2, a major non-proteolytic allergen of Dermatophagoides pteronyssinus, activates respiratory epithelial cells to produce mediators involved in asthma pathogenesis and to elucidate the mechanism of such activation.

Methods: The human bronchial epithelial cell line BEAS-2B, normal human bronchial epithelial (NHBE) cells and the alveolar epithelial cell line A549 were exposed to recombinant Der p 2. Following exposure, we analysed a panel of soluble mediators and cell adhesion receptors involved in asthma pathogenesis by promoting recruitment, survival and binding of inflammatory cells. The involvement of nuclear factor (NF)-kappaB and mitogen-activated protein kinases (MAPKs) was studied using specific inhibitors.

Results: Der p 2 activated bronchial BEAS-2B and NHBE cells, but not alveolar A549 cells. In BEAS-2B cells Der p 2 induced dose-dependent up-regulation in both mRNA level and protein secretion of granulocyte-macrophage colony-stimulating factor, IL-6, IL-8, monocyte-chemotactic protein-1 and macrophage inflammatory protein-3alpha. Secretion as well as surface expression of intercellular adhesion molecule (ICAM)-1 was also up-regulated, which was associated with increased adhesion of monocytes to the epithelial cells. The release of cytokines and chemokines was regulated by NF-kappaB and MAPK activation in different ways, while expression of ICAM-1 was solely dependent on NF-kappaB activation.

Conclusion: These results show that Der p 2 activates respiratory epithelial cells, indicating that this non-proteolytic allergen, in addition to its immunogenic properties, can aggravate respiratory airway disease by adjuvant-like activation of the lung epithelium.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, Dermatophagoides / immunology*
  • Arthropod Proteins
  • Asthma / immunology
  • Asthma / physiopathology
  • Bronchi / cytology
  • Bronchi / immunology*
  • Cells, Cultured
  • Chemokine CCL2 / metabolism
  • Chemokine CCL20 / metabolism
  • Dermatophagoides pteronyssinus / immunology
  • Epithelial Cells / immunology*
  • Granulocyte-Macrophage Colony-Stimulating Factor / metabolism
  • Humans
  • Intercellular Adhesion Molecule-1 / biosynthesis
  • Interleukin-6 / metabolism
  • Interleukin-8 / metabolism
  • Mitogen-Activated Protein Kinases / immunology*
  • NF-kappa B / immunology*
  • RNA, Messenger / immunology
  • Signal Transduction / immunology
  • Up-Regulation / immunology

Substances

  • Antigens, Dermatophagoides
  • Arthropod Proteins
  • Chemokine CCL2
  • Chemokine CCL20
  • Dermatophagoides pteronyssinus antigen p 2
  • Interleukin-6
  • Interleukin-8
  • NF-kappa B
  • RNA, Messenger
  • Intercellular Adhesion Molecule-1
  • Granulocyte-Macrophage Colony-Stimulating Factor
  • Mitogen-Activated Protein Kinases