title: Normal mesenteric lymph ameliorates lipopolysaccharide challenge-induced spleen injury.
abstract: OBJECTIVE
  This study was conducted to investigate the effect of normal mesenteric lymph (NML) from mice on the spleen injury induced by lipopolysaccharide (LPS) challenge.
  
  
  METHODS
  Mice in the LPS and LPS+NML groups received an intraperitoneal injection of LPS (35 mg/kg) and kept for 6 h.. The mice in the LPS+NML group received NML treatment at 1 h after LPS injection. Afterward, the splenic morphology, the levels of lipopolysaccharide-binding protein (LBP), cluster of differentiation 14 (CD14), phosphorylation mitogen-activated protein kinases (MAPKs), and inflammatory mediators in splenic tissue were investigated.
  
  
  RESULTS
  LPS injection induced spleen injury, increased the levels of LBP, CD14, tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), and interferon γ (IFN-γ), and decreased the IL-4 content in the spleen. By contrast, NML treatment reversed these changes. Meanwhile, the LPS challenge decreased the phosphorylation levels of p38 MAPK, extracellular regulated protein kinases 1/2, and c-Jun N-terminal kinase (JNK). Moreover, the phosphorylation levels of p38 MAPK and JNK were further decreased by the NML administration.
  
  
  CONCLUSIONS
  rRdThe normal mesenteric lymph treatment alleviated lipopolysaccharide induced spleen injury by attenuating LPS sensitization and production of TNF-α, IL-6, and IFN-γ.
authors.affiliation: Institute of Microcirculation, Hebei North University, Zhangjiakou, CN.
authors.forename: Li-min
authors.initials: LM
authors.lastname: Zhang
authors.affiliation: Institute of Microcirculation, Hebei North University, Zhangjiakou, CN.
authors.forename: Wen
authors.initials: W
authors.lastname: Song
authors.affiliation: Hebei North University, Zhangjiakou, CN.
authors.forename: Hao
authors.initials: H
authors.lastname: Cui
authors.affiliation: Institute of Microcirculation, Hebei North University, Zhangjiakou, CN.
authors.forename: Li-qiang
authors.initials: LQ
authors.lastname: Xing
authors.affiliation: Institute of Microcirculation, Hebei North University, Zhangjiakou, CN.
authors.forename: Hui-bo
authors.initials: HB
authors.lastname: Du
authors.affiliation: Hebei North University, Zhangjiakou, CN.
authors.forename: Ying
authors.initials: Y
authors.lastname: Cui
authors.affiliation: Hebei North University, Zhangjiakou, CN.
authors.forename: Wei-hong
authors.initials: WH
authors.lastname: Chen
authors.affiliation: Institute of Microcirculation, Hebei North University, Zhangjiakou, CN.
authors.forename: Zi-gang
authors.initials: ZG
authors.lastname: Zhao
authors.affiliation: Institute of Microcirculation, Hebei North University, Zhangjiakou, CN.
authors.forename: Chun-yu
authors.initials: CY
authors.lastname: Niu
mesh_terms: D000209:Acute-Phase Proteins / Q000032:analysis; D000818:Animals; D002352:Carrier Proteins / Q000032:analysis; D016207:Cytokines / Q000032:analysis; D004797:Enzyme-Linked Immunosorbent Assay; D007274:Injections, Intraperitoneal; D018950:Lipopolysaccharide Receptors / Q000032:analysis; D008070:Lipopolysaccharides / Q000008:administration & dosage*; D008198:Lymph Nodes / Q000637:transplantation*; D008562:Membrane Glycoproteins / Q000032:analysis; D008643:Mesentery; D008807:Mice, Inbred BALB C; D020929:Mitogen-Activated Protein Kinase Kinases / Q000032:analysis; D011897:Random Allocation; D015203:Reproducibility of Results; D013158:Splenic Diseases / Q000628:therapy*; D016896:Treatment Outcome; D000099231:Lipopolysaccharide-Binding Protein
chemical_list: D000209:Acute-Phase Proteins; D002352:Carrier Proteins; D016207:Cytokines; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D020929:Mitogen-Activated Protein Kinase Kinases; D000099231:Lipopolysaccharide-Binding Protein