Effects of Fungi and Eosinophils on Mucin Gene Expression in Rhinovirus-Infected Nasal Epithelial Cells.
10.4168/aair.2014.6.2.149
- Author:
Seung Heon SHIN
1
;
Mi Kyung YE
;
Jeong Kyu KIM
Author Information
1. Department of Otolaryngology, Catholic University of Daegu, School of Medicine, Daegu, Korea. hsseung@cu.ac.kr
- Publication Type:Original Article
- Keywords:
Rhinovirus;
nasal epithelial cell;
mucin gene;
fungus;
eosinophil;
nuclear factor-kappaB
- MeSH:
Alternaria;
Aspergillus;
Coculture Techniques;
Eosinophils*;
Epithelial Cells*;
Fungi*;
Gene Expression*;
Humans;
Methods;
Mucins*;
Nasal Polyps;
NF-kappa B;
Protein Kinases;
Rhinovirus;
RNA, Messenger;
Transcription Factor AP-1
- From:Allergy, Asthma & Immunology Research
2014;6(2):149-155
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Fungi, rhinoviruses (RVs), and eosinophils are associated with upper respiratory diseases. We evaluated the effects of fungal stimulation and eosinophil co-culture on the expression of mucin genes in RV-infected nasal polyp epithelial cells. METHODS: Nasal polyp epithelial cells were obtained from chronic rhinosinusitis patients. Cultured epithelial cells were stimulated with Alternaria and Aspergillus with or without RV-16 infection. The epithelial cells were co-cultured with eosinophils for 16 h. MUC4, MUC5AC, MUC5B, and MUC8 mRNA expressions in the epithelial cells were quantified using real-time RT-PCR. To determine the underlying mechanism, nuclear factor-kappaB (NF-kappaB), activator protein-1 (AP-1), and mitogen-activated protein kinase (MAPK) inhibitors were used to inhibit mucin gene expression. RESULTS: Fungi and RV-16 induced mucin gene expression in nasal polyp epithelial cells. However, there was no synergistic increase in mucin gene expression, with the exception of MUC4 mRNA expression stimulated by 25 microg/mL Aspergillus. When RV-16-infected epithelial cells were stimulated with fungi and then co-cultured with eosinophils, MUC4, MUC5B, and MUC8 mRNA expressions increased. Mucin gene expression was inhibited by NF-kappaB inhibitors. CONCLUSIONS: RV-16, airborne fungi, and eosinophils may exacerbate the inflammatory process in nasal mucosal diseases by enhancing mucin gene expression.
