Human Rhinovirus-induced Proinflammatory Cytokine and Interferon-beta Responses in Nasal Epithelial Cells From Chronic Rhinosinusitis Patients.
10.4168/aair.2015.7.5.489
- Author:
Ji Heui KIM
1
;
You Sun KIM
;
Gye Song CHO
;
Nam Hee KIM
;
Chang Hoon GONG
;
Bong Jae LEE
;
Yong Ju JANG
Author Information
1. Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. jangyj@amc.seoul.kr
- Publication Type:Original Article
- Keywords:
Chronic rhinosinusitis;
human rhinovirus;
proinflammatory cytokine;
interferon-beta;
RNA helicase
- MeSH:
Asthma;
Cytokines;
Epithelial Cells*;
Humans;
Interferon-beta*;
Interferons;
Interleukin-6;
Interleukin-8;
Rhinovirus;
RNA Helicases;
RNA, Messenger;
Turbinates
- From:Allergy, Asthma & Immunology Research
2015;7(5):489-496
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Asthma exacerbation from human rhinovirus (HRV) infection is associated with deficient antiviral interferon (IFN) secretion. Although chronic rhinosinusitis (CRS), an inflammatory upper airway disease, is closely linked to asthma, IFN-beta responses to HRV infections in human nasal epithelial cells (HNECs) from CRS patients remain to be studied. We evaluated inflammatory and antiviral responses to HRV infection in HNECs from CRS patients. METHODS: HNECs, isolated from turbinate tissue of 13 patients with CRS and 14 non-CRS controls, were infected with HRV16 for 4 hours. The HRV titer, LDH activity, production of proinflammatory cytokines and IFN-beta proteins, and expression levels of RIG-I and MDA5 mRNA were assessed at 8, 24, and 48 hours after HRV16 infection. RESULTS: The reduction in viral titer was slightly delayed in the CRS group compared to the non-CRS control group. IL-6 and IL-8 were significantly increased to a similar extent in both groups after HRV infection. In the control group, IFN-beta production and MDA5 mRNA expression were significantly increased at 8 and 24 hours after HRV16 infection, respectively. By contrast, in the CRS group, IFN-beta was not induced by HRV infection; however, HRV-induced MDA5 mRNA expression was increased, but the increase was slightly delayed compared to the non-CRS control group. The RIG-I mRNA level was not significantly increased by HRV16 infection in either group. CONCLUSIONS: HRV-induced secretion of proinflammatory cytokines in CRS patients was not different from that in the non-CRS controls. However, reductions in viral titer, IFN-beta secretion, and MDA5 mRNA expression in response to HRV infection in CRS patients were slightly impaired compared to those in the controls, suggesting that HRV clearance in CRS patients might be slightly deficient.
