Journal of Rhinology 2012;19(2):112-118.
Published online November 30, 2012.
Cooperative effect of Alternaria and rhinovirus on the activation of nasal polyp epithelial cells
Seung Heon Shin, Mi Kyung Ye, Byeong Gyu Jeon, Yong Ju Jang
1Department of Otolaryngology, Catholic University of Daegu School of Medicine, Daegu, South Korea. hsseung@cu.ac.kr
2Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.
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.
Key Words: Epithelial cell;Alternaria;Rhinovirus;Nuclear factor-kappaB;Activator protein-1


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