title: [The experimental study on the expression of toll-like receptor 2 in fulminant hepatic failure].
abstract: OBJECTIVE
  In order to explore the role of toll-like receptors 2 (TLR2) in initiating inflammatory response, the expression of TLR2 of the liver and IL-18, TNF-alpha and IFN-gamma of plasma in fulminant hepatic failure was analysed.
  
  
  METHODS
  D-galactosamine (D-Gal, 900 mg/kg) and lipopolysaccharide (LPS, 10 microg/kg) were administered intraperitoneally into the BALB/C mice. To evaluate the hepatic injury, serum transaminase (ALT and AST) and plasma IL-18, TNF-alpha and IFN-gamma were determined and the mortality was observed at various time points following the intraperitoneal injection. The level of TLR2 mRNA was measured by semiquantitative RT-PCR. The protein expression of TLR2 in the liver was detected by immunohistochemistry. The data was analyzed by SAS software.
  
  
  RESULTS
  After 4 hours of intraperitoneal injection of D-Gal/LPS, the serum transaminase and plasma IL-18, TNF-alpha and IFN-gamma levels were elevated. The treated mice began to die at 7 hours. The mortality reached up to 80% at 10 h. TLR2 mRNA was expressed at a low level in liver tissues of normal mice, while it was significantly increased and maintained at a higher level following intraperitoneal injection with D-Gal/LPS. The expression of TLR2 protein was similar to that of the TLR2 mRNA, and the expression of TLR2 mRNA was positively correlated with the concentration of plasma IL-18, TNF-alpha and IFN-gamma (r=0.36, P=0.02; r = 0.48, P 0.003; r = 0.72, P<0.001) at different time points.
  
  
  CONCLUSIONS
  Our results showed that TLR2 was involved in initiating and inducing the expression of proinflammation cytokines in this model of fulminant hepatic failure. The results suggest that adjusting the expression of TLR2 might be a new strategy in preventing the development of infectious diseases
authors.affiliation: Department of Infectious Diseases, Ruijin Hospital, Shanghai Second Medical University, Shanghai 200025, China.
authors.forename: Chun-Gen
authors.initials: CG
authors.lastname: Yan
authors.forename: Qing
authors.initials: Q
authors.lastname: Xie
authors.forename: Xia-Qiu
authors.initials: XQ
authors.lastname: Zhou
authors.forename: Yu-Min
authors.initials: YM
authors.lastname: Xu
authors.forename: Hong
authors.initials: H
authors.lastname: Yu
authors.forename: Qing
authors.initials: Q
authors.lastname: Guo
mesh_terms: D000818:Animals; D005688:Galactosamine; D007371:Interferon-gamma / Q000097:blood; D020382:Interleukin-18 / Q000097:blood; D008070:Lipopolysaccharides; D008099:Liver / Q000378:metabolism*; D017114:Liver Failure, Acute / Q000139:chemically induced / Q000378:metabolism*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051195:Toll-Like Receptor 2 / Q000096:biosynthesis* / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D020382:Interleukin-18; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D051195:Toll-Like Receptor 2; D014409:Tumor Necrosis Factor-alpha; D005688:Galactosamine; D007371:Interferon-gamma