title: [The relationship of the expression of principal pattern recognition receptor with the pulmonary injury in abdominal infection-induced sepsis].
abstract: OBJECTIVE
  In order to investigate the evidence of the synergistic effects of bacterial components, to observe the relationship of the expression of lipopolysaccharide (LPS) receptors [CD14, Toll-like receptor 4 (TLR4), scavenger receptor (SR)], lipoprotein receptor (TLR2) and bacterial DNA receptor (TLR9) with pulmonary injury in abdominal infection-induced sepsis.
  
  
  METHODS
  30 mice were used and randomly divided into cecal ligation puncture (CLP) (n = 15) and sham (n = 15) groups. The animals were respectively sacrificed 8, 12 and 24 (each point n = 5) hours following CLP and sham CLP. The lungs were removed and immediately stored in liquid nitrogen for TLRs mRNA, tumor necrosis factor (TNF) alpha and myeloperoxidase (MPO) assay. To detect the expression of CD14, TLR4, SR, TLR2 and TLR9 mRNA by reverse-transcription polymerase chain reaction, to detect the TNF-alpha content of the lung tissue by enzyme-labeled immunosorbent assay, and to assay the MPO activity of the lung tissue spectrophotometer.
  
  
  RESULTS
  It was found that the expression of receptors for LPS, BLP and bacterial DNA in pulmonary tissues was markedly changed in CLP-induced sepsis, showing upregulation of CD14 mRNA (1.143 +/- 0.139, t = 0.022, P < 0.05), TLR2 mRNA (0.418 +/- 0.102, t = 0.021, P < 0.05), TLR4 mRNA (0.595 +/- 0.052, t = 0.0001, P < 0.01) and TLR9 mRNA (0.743 +/- 0.178, t = 0.0023, P < 0.01) at different degrees (P < 0.05 or P < 0.01) after postinjury 8 h, among which the expression of TLR9 mRNA kept increasing. The expression of SR mRNA (8 h: 0.659 +/- 0.159; 12 h: 0.429 +/- 0.061; 24 h: 0.300 +/- 0.045; t = 0.029, P < 0.05; t = 0.001, P < 0.01; t = 0.003, P < 0.01) showed continuous down-regulation.
  
  
  CONCLUSIONS
  There was a marked correlation between the changes of pattern-recognition receptor expression and the increases of MPO and TNF-alpha levels in pulmonary tissues.
authors.affiliation: State Key Laboratory of Trauma, Burns and Combined Injury, Research institute for Traffic Medicine of People's Liberation Army, Department 4, Institute of Field Surgery Research, Daping Hospital, Third Military Medical University, Chongqing 400042, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Huang
authors.forename: Jian-xin
authors.initials: JX
authors.lastname: Jiang
authors.forename: Pei-fang
authors.initials: PF
authors.lastname: Zhu
authors.forename: Zheng-guo
authors.initials: ZG
authors.lastname: Wang
authors.forename: Dao-jie
authors.initials: DJ
authors.lastname: Zhang
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D008168:Lung / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D008815:Mice, Inbred Strains; D012333:RNA, Messenger / Q000235:genetics; D051192:Receptors, Pattern Recognition / Q000096:biosynthesis* / Q000235:genetics; D018805:Sepsis / Q000378:metabolism* / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D012333:RNA, Messenger; D051192:Receptors, Pattern Recognition; D014409:Tumor Necrosis Factor-alpha