Inhibitory effect of PPARγ agonists on TLR3 and TNF-α expression in human lung epithelial cells infected with respiratory syncytial virus

Objective To study the change of toll-like receptor 3 (TLR3) and tumor necrosis factoralpha (TNF-α) both at the levels of protein and mRNA in human lung epithelial cells (A549) infected with respiratory syncytial virus (RSV) and the effects of peroxisome proliferator-activated receptor γ (PPARγ) agonists Rosiglitazone and 15-deoxy-delta12,14 prostaglandin J2 (15d-PGJ2).Methods RSV inoculation after A549 cells subcultured,then A549 cells were randomly divided into six groups:15d-PGJ2 + RSV group (group A),Rosiglitazone + RSV group (group B),RSV group (group C),PDTC + RSV group (group D),GW9662 + Rosiglitazone + RSV group (group E) and cell control group (group F).Cells were harvested after incubated for 12 h,24 h and 48 h respectively.The expression of TLR3 and TNF-α at mRNA was determined by real-time RT-PCR,and the protein level of TLR3 and TNF-α was determined by Western Blot and ELISA respectively.Results The expression of TLR3 and TNF-α at mRNA and protein at virous time in group C were significantly higher than those of group F (all P ＜ 0.01).While,the expression of TLR3 and TNF-α mRNA and protein in group A,B and D were significantly lower than than those of group C (all P ＜ 0.01).15d-PGJ2 and Rosiglitazone had the strongest effect to inhibit the expression of TLR3 and TNF-αmRNA and protein at 12 h and the expression of TLR3 and TNF-α mRNA and protein decreased as the increasing dose of 15d-PGJ2 and Rosiglitazone.Conclusion RSV infection induces increased expression of TLR3 and TNF-α mRNA and protein,which can be inhibited by Rosiglitazone and 15d-PGJ2 in a dose-dependent manner. Key words: PPARγ/agonists ;  Respiratory syncytiall virus ;  Infection ;  Receptors, Toll-like ;  Tumor necrosis factor