The antiviral role of Toll-like receptor 3 in human lung epithelial cells infected with respiratory syncytial virus.
- Author:
Bao-Shun YANG
1
;
Li-Jing WANG
Author Information
- Publication Type:Journal Article
- MeSH: Epithelial Cells; immunology; virology; Humans; Interferon-alpha; genetics; Interferon-beta; genetics; Lung; immunology; virology; RNA, Messenger; analysis; Respiratory Syncytial Viruses; immunology; Time Factors; Toll-Like Receptor 3; genetics; physiology; Viral Fusion Proteins; genetics
- From: Chinese Journal of Experimental and Clinical Virology 2012;26(2):130-132
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVEIn order to understand the production mechanism of interferon and provide a scientific basis for preventionand clinical therapy, the expression changes of Toll-like receptor (TLR3) mRNA and the role of TLR3 in human lung epithelial cells (A549 cells) infected with respiratory syncytial virus (RSV) were investigated in this study.
METHODSRSV infected A549 cells were treated with or without specific antibodies of TLR3 and collected at the selected timepoints after RSV infection (4, 8, 12, 16 and 24h). The expressions of TLR3, IFN-alpha, IFN-beta and RSV F mRNA were evaluated by RT-PCR.
RESULTIt was found that RSV infection could markedly up-regulate the mRNA expression of TLR3, IFN-alpha, IFN-beta and RSV F protein in a time-dependent manner as the 24h mRNA expressions of them were 4 times, 3 times, 3 times and 0.7 times more than the basic expression, respectively. Treatment of TLR3 specific antibodies, whereas, significantly down-regulated the activation of TLR3. The mRNA expression of IFN-alpha and IFN-1beta also decreased accordingly and that of IFN-beta reduced more obviously than IFN-alpha, but that of RSV F protein rose significantly.
CONCLUSIONAbove data indicate that RSV infection could induce an apparent increase of antiviral genes of IFN-alpha and IFN-beta by activating TLR3 in human lung epithelial cells and the activated cells mediated Type I interferon is antiviral, which suggesting that TLR3 might play an important role in antiviral activity of RSV-infected human lung epithelial cells.