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Title: Peroxisome proliferator-activated receptor-{gamma} agonists inhibit the replication of respiratory syncytial virus (RSV) in human lung epithelial cells

Abstract

We have previously shown that peroxisome proliferator-activated receptor-{gamma} (PPAR{gamma}) agonists inhibited the inflammatory response of RSV-infected human lung epithelial cells. In this study, we supply evidence that specific PPAR{gamma} agonists (15d-PGJ{sub 2}, ciglitazone, troglitazone, Fmoc-Leu) efficiently blocked the RSV-induced cytotoxicity and development of syncytia in tissue culture (A549, HEp-2). All PPAR{gamma} agonists under study markedly inhibited the cell surface expression of the viral G and F protein on RSV-infected A549 cells. This was paralleled by a reduced cellular amount of N protein-encoding mRNA determined by real-time RT-PCR. Concomitantly, a reduced release of infectious progeny virus into the cell supernatants of human lung epithelial cells (A549, normal human bronchial epithelial cells (NHBE)) was observed. Similar results were obtained regardless whether PPAR{gamma} agonists were added prior to RSV infection or thereafter, suggesting that the agonists inhibited viral gene expression and not the primary adhesion or fusion process.

Authors:
 [1];  [2]
  1. Institute of Medical Microbiology, Otto-von-Guericke-University, Leipzigerstr. 44, 39120 Magdeburg (Germany). E-mail: ralf.arnold@medizin.uni-magdeburg.de
  2. Institute of Medical Microbiology, Otto-von-Guericke-University, Leipzigerstr. 44, 39120 Magdeburg (Germany)
Publication Date:
OSTI Identifier:
20850526
Resource Type:
Journal Article
Resource Relation:
Journal Name: Virology; Journal Volume: 350; Journal Issue: 2; Other Information: DOI: 10.1016/j.virol.2006.03.008; PII: S0042-6822(06)00172-3; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; GENES; INFLAMMATION; LUNGS; POLYMERASE CHAIN REACTION; PROGENY; RECEPTORS; TISSUE CULTURES; TOXICITY; VIRUSES

Citation Formats

Arnold, Ralf, and Koenig, Wolfgang. Peroxisome proliferator-activated receptor-{gamma} agonists inhibit the replication of respiratory syncytial virus (RSV) in human lung epithelial cells. United States: N. p., 2006. Web. doi:10.1016/j.virol.2006.03.008.
Arnold, Ralf, & Koenig, Wolfgang. Peroxisome proliferator-activated receptor-{gamma} agonists inhibit the replication of respiratory syncytial virus (RSV) in human lung epithelial cells. United States. doi:10.1016/j.virol.2006.03.008.
Arnold, Ralf, and Koenig, Wolfgang. Wed . "Peroxisome proliferator-activated receptor-{gamma} agonists inhibit the replication of respiratory syncytial virus (RSV) in human lung epithelial cells". United States. doi:10.1016/j.virol.2006.03.008.
@article{osti_20850526,
title = {Peroxisome proliferator-activated receptor-{gamma} agonists inhibit the replication of respiratory syncytial virus (RSV) in human lung epithelial cells},
author = {Arnold, Ralf and Koenig, Wolfgang},
abstractNote = {We have previously shown that peroxisome proliferator-activated receptor-{gamma} (PPAR{gamma}) agonists inhibited the inflammatory response of RSV-infected human lung epithelial cells. In this study, we supply evidence that specific PPAR{gamma} agonists (15d-PGJ{sub 2}, ciglitazone, troglitazone, Fmoc-Leu) efficiently blocked the RSV-induced cytotoxicity and development of syncytia in tissue culture (A549, HEp-2). All PPAR{gamma} agonists under study markedly inhibited the cell surface expression of the viral G and F protein on RSV-infected A549 cells. This was paralleled by a reduced cellular amount of N protein-encoding mRNA determined by real-time RT-PCR. Concomitantly, a reduced release of infectious progeny virus into the cell supernatants of human lung epithelial cells (A549, normal human bronchial epithelial cells (NHBE)) was observed. Similar results were obtained regardless whether PPAR{gamma} agonists were added prior to RSV infection or thereafter, suggesting that the agonists inhibited viral gene expression and not the primary adhesion or fusion process.},
doi = {10.1016/j.virol.2006.03.008},
journal = {Virology},
number = 2,
volume = 350,
place = {United States},
year = {Wed Jul 05 00:00:00 EDT 2006},
month = {Wed Jul 05 00:00:00 EDT 2006}
}