Obstructive Lung Diseases: COPD II |

A Study of Respiratory Syncytial Virus-Toll Like Receptors 3-Mediated Immune Response and the Pathogenesis of Acute Exacerbations of Chronic Obstructive Pulmonary Disease FREE TO VIEW

Shun Liu; Qian Chen; Yi Huang; Feng Wu; Ling Gong; Lan Zhu; Wei Zhang; Chuan Huang
Author and Funding Information

The Institute of Respiratory Diseases in Zunyi City, The First People's Hospital of Zunyi City, Zunyi, China

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A384. doi:10.1016/j.chest.2016.02.399
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SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: To explore whether TLR3 is a risk factors in AECOPD have been challenged viruses.

METHODS: TLR3 were detected by Real-Time polymerase chain reaction and respiratory syncytial virus (RSV) were detected by nested reverse transcription polymerase chain reaction (RT-PCR) in lower respiratory tract specimens. 20 hospitalised patients with AECOPD and 10 Normal volunteers crowd with control admitted for other reasons were studied. Then TLR3 signaling pathway was explored in the lung epithelial cells. The A549 cells were infected by different congcentration of RSV in different time, and TLR3mRNA expression was detected by RT-PCR, protein expression of TLR3 and interferon regulatory factor 3 (IRF3) were detected by Western Blot, IRF3 protein localization was measured by immunofluorescence. Interferonβ (INF-β) and interleukin 6 (IL-6) were detected in cell supernatans by ELISA.

RESULTS: 4 of the 20 AECOPD patients sample had RSV detected. FEV1% lower in was detected RSV of AECOPD than was not detected RSV of AECOPD respectively, IL-6 is higher in was detected RSV of AECOPD than was not detected RSV of AECOPD. The AECOPD group showed a increase in TLR3mRNA compared with TLR3mRNA in the control, The difference in TLR3mRNA Increase between these two groups was significant. The RSV were dected AECOPD group showed a increase in TLR3mRNA compared with the RSV were not dected AECOPD group TLR3mRNA and showed a increase obviously compared with TLR3mRNA in the control. A significant relationship between severity of reductions in lung function at exacerbation and increase in sputum TLR3 of AECOPD by significant correlations. TLR3 signaling pathway was activated in the lung epithelial cells. TLR3 mRNA/protein increases compared with the control group in A549 with RSV infctiion. IRF3 protein also increases and the occurrence of nuclear transfer in A549 with RSV infctiion. INF-β and IL-6 both were increase compared with control in RSV infected A549 cells.

CONCLUSIONS: TLR3 detection in patients with AECOPD rises. It is associated with decline in the FEV1. TLR3 may be a risk factor for virus infection in AECOPD.

CLINICAL IMPLICATIONS: This study suggest that RSV may be a pathogenic factor for AECOPD and TLR3 inducing immune response may involve in the pathogenesis of COPD.

DISCLOSURE: The following authors have nothing to disclose: Shun Liu, Qian Chen, Yi Huang, Feng Wu, Ling Gong, Lan Zhu, Wei Zhang, Chuan Huang

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