title: [Potential role of JAK/STAT in regulating Toll-like receptor 2 gene expression in rats with postburn Staphylococcus aureus sepsis].
abstract: OBJECTIVE
  To investigate the potential role of Janus kinase/signal transducers and activators of transcription (JAK/STAT) signal transduction pathway in regulating Toll-like receptor 2 (TLR2) gene expression in postburn Staphylococcus aureus infection.
  
  
  METHODS
  Thirty-eight male Wistar rats were randomly divided into four groups as follows: normal control group (n=6), postburn sepsis group (n=12), AG490 treatment group (n=10) and Rapamycin (RPM) treatment group (n=10). Tissue samples from the liver, kidneys and lungs were collected to determine TLR2 and TNF-alpha mRNA expressions.
  
  
  RESULTS
  It was found that, 0.5 and 2 hours after Staphylococcus aureus challenge, TLR2 mRNA expressions in the liver, kidneys and lungs from postburn septic animals were up-regulated rapidly (P<0.05 or P<0.01). Treatment with RPM could effectively inhibit TLR2 mRNA expressions in the liver and kidneys. However, TLR2 mRNA expressions in the above tissues from AG490 treated animals had no significant differences with those from normal controls. Two hours after Staphylococcus aureus challenge, TNF-alpha mRNA expressions in the liver, kidneys and lungs were also increased markedly (all P<0.01). Both treatment with RPM and AG490 could significantly inhibit the up-regulation of all tissue TNF-alpha mRNA expressions (P<0.05 or P<0.01), and AG490 were more significant in liver and kidneys (both P<0.01).
  
  
  CONCLUSIONS
  It is suggested that scald injury combined with Staphylococcus aureus infection can up-regulate TLR2 expression, which appears to be associated with the signal transduction of STAT.
authors.affiliation: Burns Institute, 304th Hospital of People's Liberation Army, Beijing 100037, China.
authors.forename: Hong-yun
authors.initials: HY
authors.lastname: Li
authors.forename: Yong-ming
authors.initials: YM
authors.lastname: Yao
authors.forename: Sheng
authors.initials: S
authors.lastname: Yao
authors.forename: Ning
authors.initials: N
authors.lastname: Dong
authors.forename: Yan
authors.initials: Y
authors.lastname: Yu
authors.forename: Zhi-yong
authors.initials: ZY
authors.lastname: Sheng
mesh_terms: D000818:Animals; D002056:Burns / Q000150:complications* / Q000235:genetics; D004268:DNA-Binding Proteins / Q000378:metabolism; D004195:Disease Models, Animal; D015870:Gene Expression; D007668:Kidney / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008168:Lung / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000235:genetics*; D011505:Protein-Tyrosine Kinases / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D011956:Receptors, Cell Surface / Q000235:genetics*; D018805:Sepsis / Q000209:etiology*; D015398:Signal Transduction / Q000502:physiology; D013203:Staphylococcal Infections / Q000209:etiology*; D051195:Toll-Like Receptor 2; D051193:Toll-Like Receptors; D015534:Trans-Activators / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D004268:DNA-Binding Proteins; D008562:Membrane Glycoproteins; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; C495343:Tlr2 protein, rat; D051195:Toll-Like Receptor 2; D051193:Toll-Like Receptors; D015534:Trans-Activators; D014409:Tumor Necrosis Factor-alpha; D011505:Protein-Tyrosine Kinases