title: Experimental bone marrow failure in mice ameliorated by OCH via tippling the balance of released cytokines from Th1 to Th2.
abstract: BACKGROUND
  OCH was reported to stimulate natural killer T (NKT) cells to produce predominantly T helper type 2 (Th2) cytokines. The present study was attempted to evaluate potential protection of OCH on acquired bone marrow failure syndromes (BMFS) in mice model.
  
  
  METHODS
  BMFS in mice model was established by exposure to sublethal irradiation followed by infusion with 5 × 10(6) B6 lymph nodes cells. Mice were injected intraperitoneally (I.P.) with either OCH or α-galactosylceramide (α-GC) at a dose of 100 µg kg(-1) twice a week for two weeks after post-irradiation. The control mice were I.P. with vehicle alone (10% dimethyl sulfoxide in phosphate-buffered saline). Meanwhile, anti-interleukin-4 (anti-IL-4) monoclonal antibody (mAb) (500 µg/animal) was given I.P. 2 hours prior to vehicle or OCH administration. Both interferon-γ (IFN-γ) and IL-4 levels in the serum were measured by enzyme-linked immunosorbent assay. Colony-forming unit-granulocyte-macrophage (CFU-GM) by bone marrow (BM) mononuclear cells was counted. The percentage of NKT cell in BM cells and intracellular cytokines were determined by flow cytometry.
  
  
  RESULTS
  The treatment of OCH in vivo decreased the IFN-γ/IL-4 ratio in the serum, and increased the transformation of NKT cells into NKT2 cells. The treatment of OCH in vitro increased the colonies of CFU-GM.
  
  
  CONCLUSIONS
  Our data suggests that OCH ameliorated immune-mediated BMFS in CByB6F1 mice via activation of NKT cells, and shifting the balance from Th1 to Th2.
authors: Department of Paediatrics, School of Medicine, Tongji University, Shanghai, China.
authors: Xiaohong
authors: X
authors: Qiao
authors: Xiaotian
authors: X
authors: Xie
authors: Shayi
authors: S
authors: Jiang
authors: Wei
authors: W
authors: Shi
authors: Jinqing
authors: J
authors: Tang
authors: Nina
authors: N
authors: Zhou
mesh_terms: D000741:Anemia, Aplastic; D000818:Animals; D001854:Bone Marrow Cells / Q000276:immunology* / Q000378:metabolism; D001855:Bone Marrow Diseases; D000080983:Bone Marrow Failure Disorders; D016207:Cytokines / Q000097:blood / Q000276:immunology*; D005260:Female; D006017:Glycolipids / Q000494:pharmacology*; D006457:Hemoglobinuria, Paroxysmal / Q000097:blood / Q000178:diet therapy* / Q000276:immunology / Q000473:pathology; D018655:Lymphocyte Count; D051379:Mice; D008807:Mice, Inbred BALB C; D055611:Natural Killer T-Cells / Q000276:immunology* / Q000378:metabolism; D018417:Th1 Cells / Q000276:immunology* / Q000378:metabolism; D018418:Th2 Cells / Q000276:immunology* / Q000378:metabolism; D014916:Whole-Body Irradiation
chemical_list: D016207:Cytokines; D006017:Glycolipids; C501055:tetracosanoic acid 1-galactopyranosyloxy-3,4-dihydroxydec-2-yl amide