title: [Endoplasmic reticulum stress collaborates with lipopolysaccharide to promote the inflammatory response in macrophages].
abstract: OBJECTIVE
  To investigate the protective mechanism of endoplasmic reticulum stress (ERS) inhibition against inflammation-induced acute liver injury using a mouse model.
  
  
  METHODS
  Marrow-derived stem cells were isolated from mouse femur and used to derive macrophages for analysis in experimental inflammation conditions, established by exposure to LPS and consequent activation of TLR4. Tunicamycin, an ERS chemical inducer, was applied to interfere the inflammation model condition.Affect on the inflammation-related factor MAPK was detected by western blot, and affects on gene expression of inflammatory factors were measured by real-time quantitative PCR. Affect on TNFa was also measured by ELISA.
  
  
  RESULTS
  Expression of TNFa, IL-6 and IL-1b was induced upon exposure to LPS, with the peak levels being reached at 4 hours of exposure (TNFa, 0.82+/-0.24; IL-1 b, 2.20+/-0.69; IL-6, 0.330+/-0.150). Tunicamycin significantly enhanced the LPS-induced up-regulation of TNFa, IL-6 and IL-1b expression (TNFa, 1.44+/-0.38, t=2.8, P<0.05; IL-1b, 16.063.40, t =7.93, P<0.05; IL-6, 31.1610.60, t=5.08, P<0.05). The tuniamycin treatment also enhanced the LPS-induced up-regulation of the protein expression of phospo-p38, phospho-JNK and phoshpo-ERK.
  
  
  CONCLUSIONS
  ERS collaborates with LPS to promote the TLR4-mediated inflammatory response of macrophages, and this collaboration may be a pathogenic mechanism underlying progressive development of acute liver injury.
authors.affiliation: Beijing You'an Hospital, Affiliated to Capital Medical University, Beijing 100069, China.
authors.forename: Xianghua
authors.initials: X
authors.lastname: Guo
authors.forename: Feng
authors.initials: F
authors.lastname: Ren
authors.forename: Xiangying
authors.initials: X
authors.lastname: Zhang
authors.forename: Hongbo
authors.initials: H
authors.lastname: Shi
authors.forename: Dexi
authors.initials: D
authors.lastname: Chen
authors.forename: Zhongping
authors.initials: Z
authors.lastname: Duan
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D059865:Endoplasmic Reticulum Stress; D007249:Inflammation; D015850:Interleukin-6; D008070:Lipopolysaccharides; D008099:Liver; D008264:Macrophages; D051379:Mice; D051197:Toll-Like Receptor 4; D015854:Up-Regulation
chemical_list: D015850:Interleukin-6; D008070:Lipopolysaccharides; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4