Toll-like receptors expression in the lungs of human metapneumovirus infected mice and the effects of polyI:C on viral infection.
- Author:
Ying DOU
1
;
Yao ZHAO
;
Zhi-Yong ZHANG
;
Xiao-Dong ZHAO
Author Information
1. P2 Lab Children's Hospital Chongqing Medical University, Chongqing 400014, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Disease Models, Animal;
Female;
Gene Expression;
Humans;
Lung;
drug effects;
metabolism;
virology;
Metapneumovirus;
drug effects;
genetics;
physiology;
Mice;
Mice, Inbred BALB C;
Paramyxoviridae Infections;
drug therapy;
genetics;
metabolism;
virology;
Poly I-C;
therapeutic use;
Toll-Like Receptors;
genetics;
metabolism;
Virus Replication
- From:
Chinese Journal of Virology
2010;26(1):1-7
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the expression changes of Toll-like receptors (TLR) in the lungs of human metapneumovirus infected BALB/c mice, and to explore the effects of PolyI:C on viral replication, HMPV-infected group, PolyI:C+hMPV group, PolyI:C+DMED group and DMEM control group were set up for this study. All mice were sacrificed on day 1, 3, 5, 7, 9 and 16 post inoculation. Lungs were used for viral titration, pulmonary histopathology and detection of TLRs mRNA expression by RT-PCR and real-time PCR. Results showed that the levels of viral replication in the lungs of PolyI:C+hMPV infected mice were significantly decreased and lung inflammation were also lessened compared with those of hMPV infected mice. RT-PCR detection showed that mRNA levels of most TLRs were up-regulated (P < 0.05) in the lungs of hMPV infected group compared with DMEM group. Real time PCR assay showed that TLR7-8 mRNA significantly increased in hMPV infected group in a time-dependent manner. The level of TLR3 mRNA was significantly up-regulated in PolyI:C+hMPV group at the 24 hour after intranasal inoculation. The results showed that hMPV infection up-regulated the expression of TLRs in lungs of BALB/c mice and TLR7/8 pathway might play an important role in the start of natural immune response. PolyI:C was capable of inhibiting viral replication in the lung of mice and reducing lung inflammation probably through the early activation of TLR3.
