title: Increased serum endotoxin and elevated CD14 and IL-1beta expression in a rat model of cerebrogenic multiple organ dysfunction syndrome.
abstract: OBJECTIVE
  To study the mechanisms underlying cerebrogenic multiple organ dysfunction syndrome (CMODS) through investigation of endotoxin levels and the expression of endotoxin receptor CD14 and interleukin IL-1beta mRNAs in a rat CMODS model.
  
  
  METHODS
  Acute cerebral hemorrhage was induced in Wistar rats by focal intracerebral injection of collagenase into the caudate nucleus. Serum endotoxin levels were quantitated using a chromogenic limulus lysate method; CD14 endotoxin receptor mRNA and IL-1beta mRNA levels in lung and intestine were determined by in situ hybridization.
  
  
  RESULTS
  Serum endotoxin levels increased after 12 h, reaching a peak after 24 h, and declined to control levels at 72 h. The increase was statistically significant (P<0.05) compared to unoperated controls and the sham-operated group respectively. CD14 mRNA in lung and intestine increased after 12 h, peaked after 24-36 h, and then declined after 48 h. IL-1beta mRNA levels were also increased in lung and intestine (P<0.05), peaking at 36 h and declining thereafter. Expression levels of both CD14 and IL-1beta mRNAs correlated significantly with serum endotoxin levels (Plt;0.01). We conclude that acute cerebral hemorrhage results in endotoxemia and widespread increases in CD14 and IL-1beta expression. We suggest that acute cerebrovascular challenge leads to a stress/shock response that compromises the intestinal mucosal barrier. In turn, this allows endotoxin translocation into the body that provokes the release of pro-inflammatory lymphokines, leading to a systemic inflammatory response syndrome (SIRS) that culminates in multiple organ dysfunction.
authors.affiliation: Department of Neurology, Qilu Hospital, Shandong University, Jinan, 250021, China.
authors.forename: Chuanqiang
authors.initials: C
authors.lastname: Qu
authors.forename: Shougang
authors.initials: S
authors.lastname: Guo
authors.forename: Hongzhi
authors.initials: H
authors.lastname: Guo
authors.forename: Chunjuan
authors.initials: C
authors.lastname: Wang
authors.forename: Lin
authors.initials: L
authors.lastname: Ma
authors.forename: Yan
authors.initials: Y
authors.lastname: He
authors.forename: Lei
authors.initials: L
authors.lastname: Wang
authors.forename: Jianwei
authors.initials: J
authors.lastname: Lou
authors.forename: Xingbang
authors.initials: X
authors.lastname: Wang
mesh_terms: D000818:Animals; D002543:Cerebral Hemorrhage / Q000150:complications; D004195:Disease Models, Animal; D004731:Endotoxins / Q000097:blood*; D005786:Gene Expression Regulation; D053583:Interleukin-1beta / Q000235:genetics*; D018950:Lipopolysaccharide Receptors / Q000235:genetics*; D008297:Male; D009102:Multiple Organ Failure / Q000097:blood* / Q000175:diagnosis / Q000209:etiology / Q000235:genetics*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D055986:Vital Signs
chemical_list: D004731:Endotoxins; D053583:Interleukin-1beta; D018950:Lipopolysaccharide Receptors; D012333:RNA, Messenger