Document Detail


Asian sand dust enhances rhinovirus-induced cytokine secretion and viral replication in human nasal epithelial cells.
MedLine Citation:
PMID:  20879958     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
CONTEXT: Asian sand dust (ASD) originating in the arid deserts of Mongolia and China causes annual severe air pollution events in the Asia-Pacific area, including Korea, Japan, and China. ASD is thought to impact public health by aggravating or inducing respiratory illness. Among the most common respiratory illnesses is the common cold caused by rhinovirus (RV) infection. To date, however, the impact of ASD on RV infection has not been studied.
OBJECTIVE: In this study, we investigated the effect of ASD on RV infection in human nasal epithelial cells.
METHODS: Primary human nasal epithelial cells grown at an air-liquid interface were treated with ASD and/or RV. After RV infections were confirmed using semi-nested reverse transcription-polymerase chain reaction (RT-PCR), mRNA expression and protein secretion of the inflammatory cytokines interferon-γ (IFN-γ), interleukin-1β (IL-1β),IL-6, and IL-8, indicators of the severity of RV-induced inflammation, were measured by real-time PCR and enzyme-linked immunosorbent assays. Viral titer was also assayed by culturing viruses to compare viral replication between RV-only and ASD-plus-RV groups.
RESULTS: ASD significantly increased RV-induced IFN-γ, IL-1β, IL-6, and IL-8 mRNA levels and protein secretion in primary nasal epithelial cells. In addition, ASD caused a significant increase in RV replication.
CONCLUSIONS: Our results suggest that ASD may potentiate common cold symptoms associated with RV infection not only by enhancing IFN-γ, IL-1β, IL-6, and IL-8 secretion, but also by increasing viral replication.
Authors:
Nam-Kyung Yeo; You-Jin Hwang; Seon-Tae Kim; Hyun Ja Kwon; Yong Ju Jang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Inhalation toxicology     Volume:  22     ISSN:  1091-7691     ISO Abbreviation:  Inhal Toxicol     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-09-30     Completed Date:  2011-01-11     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8910739     Medline TA:  Inhal Toxicol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1038-45     Citation Subset:  IM    
Affiliation:
Department of Otolaryngology, Gangneung Asan Hospital, University of Ulsan College of Medicine, Gangneung, Korea.
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MeSH Terms
Descriptor/Qualifier:
Administration, Intranasal
Air Pollutants / chemistry,  immunology,  toxicity*
Air Pollution / adverse effects
Cells, Cultured
Cytokines / genetics,  metabolism
Dust / analysis*
Gene Expression / drug effects
Humans
Inhalation Exposure / adverse effects
Nasal Mucosa / drug effects*,  immunology,  virology
Picornaviridae Infections / chemically induced*,  immunology,  virology
RNA, Messenger / metabolism
Rhinovirus / physiology
Silicon Dioxide / chemistry,  immunology,  toxicity*
Virus Replication / drug effects*,  immunology
Chemical
Reg. No./Substance:
0/Air Pollutants; 0/Cytokines; 0/Dust; 0/RNA, Messenger; 7631-86-9/Silicon Dioxide

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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