title: [Effect of carbachol on dendritic cell function in the lipopolysaccharides induced murine sepsis model].
abstract: OBJECTIVE
  To explore the mechanism of the effect of carbachol in the treatment of sepsis at the angle of modulation of dendritic cell (DC) activity.
  
  
  METHODS
  Thirty male C57BL/6 mice were randomized into three groups: normal control, sepsis and carbachol. The sepsis model of mice was reproduced by the injection of lipopolysaccharides (LPS). The expression of interleukin-1 beta (IL-1 beta) and IL-12 p70 positive cells were measured by immunohistochemistry method. The changes in DC activity in the spleen of mice were studied using flow cytometry.
  
  
  RESULTS
  In LPS group, the number of splenic DC was increased, but it was not statistically significant. The expression of DC molecules including major histocompatibility complex-II (MHC-II), CD86 and the rate of positive cells containing IL-1 beta and IL-12 p70 were significantly higher than those in normal controls (all P<0.05). While in carbachol treatment group, the number of splenic DC had no significant change, the expression of IL-1 beta was down-regulated, dramatically. The expression of MHC-II, CD86 and IL-12 p70 were also lowered (all P<0.05).
  
  
  CONCLUSIONS
  Carbachol can lower the DC activity, suggesting that modulation of DC activity may lower extensive immune and inflammatory response in the early phases of sepsis.
authors.affiliation: Department of Pathology, Burn Institute, First Affiliated Hospital of General Hospital of PLA, Beijing 100037, China.
authors.forename: Guang
authors.initials: G
authors.lastname: Tian
authors.forename: Jiang-yang
authors.initials: JY
authors.lastname: Lu
authors.forename: Sen
authors.initials: S
authors.lastname: Hu
authors.forename: Yi
authors.initials: Y
authors.lastname: Lü
authors.forename: Hong-wei
authors.initials: HW
authors.lastname: Wang
authors.forename: Yi
authors.initials: Y
authors.lastname: Yang
mesh_terms: D000818:Animals; D051940:B7-2 Antigen / Q000276:immunology / Q000378:metabolism; D039521:CD11c Antigen / Q000276:immunology / Q000378:metabolism; D002217:Carbachol / Q000494:pharmacology*; D003713:Dendritic Cells / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D004195:Disease Models, Animal; D005802:Genes, MHC Class II / Q000276:immunology; D018664:Interleukin-12 / Q000276:immunology / Q000378:metabolism; D053583:Interleukin-1beta / Q000276:immunology / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D011897:Random Allocation; D018805:Sepsis / Q000139:chemically induced / Q000276:immunology* / Q000378:metabolism; D013154:Spleen / Q000276:immunology / Q000378:metabolism
chemical_list: D051940:B7-2 Antigen; D039521:CD11c Antigen; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D018664:Interleukin-12; D002217:Carbachol