title: Upregulation of TLR7 and TLR3 gene expression in the lung of respiratory syncytial virus infected mice.
abstract: OBJECTIVE
  TLR7 and TLR3 (Toll-like receptor, TLR) are important pattern recognition receptors (PRRs) that recognize the single-strand RNA and double-strand RNA of virus-origin. Respiratory syncytial virus (RSV) could be recognized by both TLR7 and TLR3. We studied the kinetics and profile of lung TLR7 and TLR3 expression during the early phase of the RSV infection, and explored their expression correlation with pulmonary inflammatory response.
  
  
  METHODS
  We intranasally inoculated BALB/c mice with live RSV to induce acute lung inflammation,and detected the lung expression of TLR7 and TLR3 mRNA by semiquantitative RT-PCR analysis at day 1 after RSV infection. We also measured the transcription factor nuclear factor-kappaB (NF-kappaB) protein expression with western blot assay in nuclear extracts. Lung tissue sections were stained with hematoxylin and eosin, and examined under a light microscope for histopathological examination.
  
  
  RESULTS
  SV infection could rapidly upregulate the lung expression levels of both TLR7 and TLR3 gene in a time-dependent manner. Furthermore, the response of TLR7 to RSV (1 h) was prior to that of TLR3 (4 h). It resulted in activation of NF-kappaB as soon as 4 h later in lung tissue. Moreover, RSV mediated early transcriptional responses of TLR7 and TLR3 were paralleling with the severe extent of RSV-induced pulmonary inflammation.
  
  
  CONCLUSIONS
  TLR7 and TLR3 were really involved in RSV-induced lung inflammation by detecting the viral RNA. This may allow to detect viral infections and initiate a proinflammatory response via multiple TLRs. This study may be useful in the development of tools to modulate the activities of therapeutic TLR ligands.
authors.affiliation: Department of Microbiology, 2 Institute of Clinical Pharmacology, Key Laboratory of Antiinflammatory and Immunopharmacology in Anhui Province, Anhui Medical University, Hefei 230032, China. shhuang@ahmu.edu.cn
authors.forename: Shenghai
authors.initials: S
authors.lastname: Huang
authors.forename: Wei
authors.initials: W
authors.lastname: Wei
authors.forename: Yun
authors.initials: Y
authors.lastname: Yun
mesh_terms: D000818:Animals; D005260:Female; D015870:Gene Expression; D006801:Humans; D008168:Lung / Q000378:metabolism* / Q000821:virology; D008562:Membrane Glycoproteins / Q000235:genetics* / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D016328:NF-kappa B / Q000235:genetics / Q000276:immunology; D018357:Respiratory Syncytial Virus Infections / Q000235:genetics* / Q000276:immunology / Q000821:virology; D012136:Respiratory Syncytial Viruses / Q000502:physiology*; D051196:Toll-Like Receptor 3 / Q000235:genetics* / Q000276:immunology; D051199:Toll-Like Receptor 7 / Q000235:genetics* / Q000276:immunology; D015854:Up-Regulation
chemical_list: D008562:Membrane Glycoproteins; D016328:NF-kappa B; C519703:TLR3 protein, mouse; C477038:Tlr7 protein, mouse; D051196:Toll-Like Receptor 3; D051199:Toll-Like Receptor 7