Th2 Responses Elicited by Nasal Epithelial Cells Exposed to House Dust Mite Extract.
- Author:
Seung Heon SHIN
1
;
Mi Kyung YE
Author Information
- Publication Type:Original Article
- Keywords: House dust mite; Nasal epithelial cell; Peripheral blood mononuclear cell; Cytokine; Intercellular adhesion molecule
- MeSH: Allergens; Cell Membrane; Colony-Stimulating Factors; Dermatophagoides pteronyssinus; Dust; Epithelial Cells; Immune System; Inflammation; Intercellular Adhesion Molecule-1; Interferon-gamma; Interleukin-5; Interleukins; Nasal Polyps; Pyroglyphidae; RNA, Messenger; Tumor Necrosis Factor-alpha
- From:Clinical and Experimental Otorhinolaryngology 2009;2(4):175-180
- CountryRepublic of Korea
- Language:English
- Abstract: OBJECTIVES: Respiratory epithelial cells are the first site of interaction of allergens with the immune system. The aim of this study was to examine the effect of epithelial cells, which were stimulated with house dust mite (HDM) extracts, on the immune response of peripheral blood mononuclear cells (PBMCs). METHODS: Primary nasal polyp epithelial cells were exposed to dermatophagoides pteronyssinus and dermatophagoides farina for 48 hr, and then the supernatant and cells were collected. After stimulation with HDM extract, the epithelial cells were co-cultured with PBMCs for 72 hr and then the supernatant was collected. We measured the interleukin (IL)-8 and granulocyte-macrophage colony stimulating factor to determine the activation of the epithelial cells. The tumor necrosis factor (TNF)-alpha, IL-5 and interferon-gamma were measured to evaluate the interaction between the epithelial cells and the PBMCs. The mRNA expression of intercellular adhesion molecule 1 (ICAM-1) was assessed using the anti-ICAM-1 antibody. RESULTS: The HDM extracts activated the nasal epithelial cells and enhanced the expression of ICAM-1 mRNA and cell membrane ICAM-1. When the activated epithelial cells were co-cultured with PBMCs, the PBMCs produced lager amounts of TNF-alpha and IL-5. However the cytokine production was not inhibited by pretreatment with ICAM-1 antibody. CONCLUSION: HDM allergens induce allergic inflammation by activating nasal epithelial cells, yet the interaction of the epitheila cells and the PBMCs may not be associated with an ICAM-1 medicated mechanism.
