PMID- 29845280
OWN - NLM
STAT- MEDLINE
DCOM- 20181018
LR  - 20181018
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Linking)
VI  - 18
IP  - 2
DP  - 2018 Aug
TI  - Oxidative stress modulates the expression of toll‑like receptor 3 during 
      respiratory syncytial virus infection in human lung epithelial A549 cells.
PG  - 1867-1877
LID - 10.3892/mmr.2018.9089 [doi]
AB  - Toll‑like receptor 3 (TLR3) can react with double stranded RNA and is involved in 
      the inflammatory response to respiratory syncytial virus (RSV) infection. Also, 
      oxidative stress has been reported to be involved in RSV infection. However, the 
      correlation between oxidative stress and TLR3 activation during RSV infection is 
      unclear. Therefore, the present study investigated the association between TLR3 
      expression and oxidative stress modulation during RSV infection in A549 cells. 
      For comparison, seven treatment groups were established, including RSV‑treated 
      cells, N‑acetyl‑L‑cysteine (NAC)+RSV‑treated cells, oxidant hydrogen peroxide 
      (H2O2)+RSV‑treated cells, normal cell control, inactivated RSV control, NAC 
      control and H2O2 control. The mRNA expression changes of TLR3, interferon 
      regulatory factor‑3 (IRF3), nuclear factor‑kappaB (NF‑kappaB) and superoxide dismutase 
      1 (SOD1) were measured using semi‑quantitative reverse transcription‑polymerase 
      chain reaction, and the protein changes of TLR3 and phospho‑NF‑kappaB p65 were 
      determined using western blot in A549 cells from the different treatment groups. 
      The present study also evaluated the differences in hydroxyl free radical (.OH), 
      nitric oxide (NO) and total SOD activity in the different treatment groups. The 
      results demonstrated that RSV infection of A549 cells increased the levels of .OH 
      and NO, while decreasing the activity of total SOD. Pretreatment of A549 cells 
      with H2O2 prior to RSV infection upregulated the mRNA and protein expression of 
      TLR3 and NF‑kappaB, and downregulated the mRNA expression of IRF3 and SOD1, as well 
      as the total SOD activity. When the infected cells were pretreated with NAC, the 
      mRNA and protein expression of these genes were reversed. These variations in the 
      TLR3‑mediated signaling pathway molecules suggested that oxidative stress may be 
      a key regulator for TLR3 activation during RSV infection. RSV‑induced oxidative 
      stress may potentially activate TLR3 and enhance TLR3‑mediated inflammation. 
      These results may provide better understanding of the RSV‑induced inflammatory 
      and immune pathways, and may also contribute to the drug development and 
      prevention of human RSV diseases.
FAU - Wang, Min-Min
AU  - Wang MM
AD  - Department of Microbiology, School of Basic Medical Sciences, Anhui Medical 
      University, Hefei, Anhui 230032, P.R. China.
FAU - Lu, Min
AU  - Lu M
AD  - Department of Laboratory, The First Affiliated Hospital of Anhui Medical 
      University, Hefei, Anhui 230032, P.R. China.
FAU - Zhang, Chuan-Long
AU  - Zhang CL
AD  - Department of Pediatrics, The People's Hospital of Lu'an City, Lu'an, Anhui 
      237005, P.R. China.
FAU - Wu, Xuan
AU  - Wu X
AD  - Department of Microbiology, School of Basic Medical Sciences, Anhui Medical 
      University, Hefei, Anhui 230032, P.R. China.
FAU - Chen, Jing-Xian
AU  - Chen JX
AD  - Department of Microbiology, School of Basic Medical Sciences, Anhui Medical 
      University, Hefei, Anhui 230032, P.R. China.
FAU - Lv, Wei-Wei
AU  - Lv WW
AD  - Department of Microbiology, School of Basic Medical Sciences, Anhui Medical 
      University, Hefei, Anhui 230032, P.R. China.
FAU - Sun, Tao
AU  - Sun T
AD  - Department of Microbiology, School of Basic Medical Sciences, Anhui Medical 
      University, Hefei, Anhui 230032, P.R. China.
FAU - Qiu, Huan
AU  - Qiu H
AD  - Department of Microbiology, School of Basic Medical Sciences, Anhui Medical 
      University, Hefei, Anhui 230032, P.R. China.
FAU - Huang, Sheng-Hai
AU  - Huang SH
AD  - Department of Microbiology, School of Basic Medical Sciences, Anhui Medical 
      University, Hefei, Anhui 230032, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20180529
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (TLR3 protein, human)
RN  - 0 (Toll-Like Receptor 3)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 3352-57-6 (Hydroxyl Radical)
RN  - EC 1.15.1.1 (Superoxide Dismutase-1)
SB  - IM
MH  - A549 Cells
MH  - Epithelial Cells/virology
MH  - Gene Expression Regulation/genetics
MH  - Humans
MH  - Hydroxyl Radical/metabolism
MH  - Lung/pathology/virology
MH  - Nitric Oxide/genetics
MH  - Oxidative Stress/*genetics
MH  - Respiratory Syncytial Virus Infections/*genetics/pathology/virology
MH  - Respiratory Syncytial Viruses/*pathogenicity
MH  - Superoxide Dismutase-1/genetics
MH  - Toll-Like Receptor 3/*genetics
EDAT- 2018/05/31 06:00
MHDA- 2018/10/20 06:00
CRDT- 2018/05/31 06:00
PHST- 2017/04/29 00:00 [received]
PHST- 2018/05/11 00:00 [accepted]
PHST- 2018/05/31 06:00 [pubmed]
PHST- 2018/10/20 06:00 [medline]
PHST- 2018/05/31 06:00 [entrez]
AID - 10.3892/mmr.2018.9089 [doi]
PST - ppublish
SO  - Mol Med Rep. 2018 Aug;18(2):1867-1877. doi: 10.3892/mmr.2018.9089. Epub 2018 May 
      29.