Cooperative effect of Alternaria and rhinovirus on the activation of nasal polyp epithelial cells.
- Author:
Seung Heon SHIN
1
;
Mi Kyung YE
;
Byeong Gyu JEON
;
Yong Ju JANG
Author Information
1. Department of Otolaryngology, Catholic University of Daegu School of Medicine, Daegu, South Korea. hsseung@cu.ac.kr
- Publication Type:Original Article
- Keywords:
Epithelial cell;
Alternaria;
Rhinovirus;
Nuclear factor-kappaB;
Activator protein-1
- MeSH:
Allergens;
Alternaria;
Blotting, Western;
Cytokines;
Enzyme-Linked Immunosorbent Assay;
Epithelial Cells;
Granulocyte-Macrophage Colony-Stimulating Factor;
Granulocytes;
Inflammation;
Interleukin-6;
Interleukin-8;
Interleukins;
Macrophage Colony-Stimulating Factor;
Nasal Mucosa;
Nasal Polyps;
NF-kappa B;
Protein Kinases;
Rhinovirus;
Transcription Factor AP-1;
Transcription Factors
- From:Journal of Rhinology
2012;19(2):112-118
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND AND OBJECTIVES: The nasal epithelium is the first barrier encountered by airborne allergens and is an active participant in airway inflammation. The aim of this study was to determine the activation mechanism of nasal epithelial cells with Alternaria and the effect of rhinovirus on the Alternaria induced activation of nasal epithelial cells. MATERIALS AND METHODS: Cultured epithelial cells were stimulated by Alternaria with or without rhinovirus-16 (RV-16) infection. Release of interleukin (IL)-6, IL-8, and granulocyte macrophage colony-stimulating factor (GM-CSF) into culture supernatants were measured to determine the activation of epithelial cells. Nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1) of the epithelial cells were analyzed using western blot analysis. Intracellular NF-kappaB and AP-1 activity were evaluated by enzyme-linked immunosorbent assay. To determine the epithelial cell activation mechanism, cytokine production was inhibited with NF-kB, AP-1, and mitogen activated protein kinase (MAPK) inhibitors. RESULTS: Exposure of epithelial cells to Alternaria enhanced the production of cytokines. Intracellular NF-kB expression and activity were significantly increased by Alternaria, but not by RV-16. AP-1 expression and activity were not influenced by Alternaria. Increased IL-6 production was significantly inhibited by transcription factor inhibitors. However, IL-8 and GM-CSF production were not inhibited by these transcription factor inhibitors. CONCLUSIONS: Our in-vitro results demonstrate that Alternaria activates nasal polyp epithelial cells via NF-kB pathway and that NF-kB, AP-1, and MAPK are involved in the production of IL-6.
