title: The lipopolysaccharide-induced pro-inflammatory response in RAW264.7 cells is attenuated by an unsaturated fatty acid-bovine serum albumin complex and enhanced by a saturated fatty acid-bovine serum albumin complex.
abstract: OBJECTIVE
  A 1:1 ratio of fatty acid (FA)-albumin complex was chosen to mimic physiological conditions, and the effects of FA-bovine serum albumin (BSA) complexes were tested in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophage cells.
  
  
  METHODS
  Nitric oxide (NO) and various proteins/factors in RAW264.7 cells were quantified as follows: NO by the Griess assay; prostaglandin (PG) E(2), interleukin (IL)-6 and tumor necrosis factor (TNF)-α by ELISA; inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 by Western blotting; and NF-κB and CD14/TLR4 by Western blotting or flow cytometry.
  
  
  RESULTS
  BSA- or FA-BSA-treated RAW264.7 cells without LPS stimulation did not show any significant changes in NO or the tested proteins/factors and thus did not have any pro-inflammatory responses. Pre-treatment with unsaturated FA-BSA complexes significantly decreased the production of LPS-induced NO, PGE(2), IL-6 and TNF-α, the expression of iNOS, COX-2 and CD14, IκB degradation and NF-κB translocation. On the contrary, pre-treatment with saturated FA-BSA complexes enhanced these LPS-induced pro-inflammatory factors and the subsequent responses.
  
  
  CONCLUSIONS
  We concluded that unsaturated FA-BSA complexes, but not saturated FA-BSA complexes, exert an inhibitory effect on the LPS-induced pro-inflammatory response and that this effect may be partially mediated through suppression of the NF-κB signaling pathway. We suggest that an increase of unsaturated FA-BSA complexes may enhance the host's defense against bacterial infection.
authors.affiliation: Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, 1-1, Jen-Ai Road, Taipei, 100, Taiwan.
authors.forename: Chi Fen
authors.initials: CF
authors.lastname: Chang
authors.forename: Yat Pang
authors.initials: YP
authors.lastname: Chau
authors.forename: Hsiu Ni
authors.initials: HN
authors.lastname: Kung
authors.forename: Kuo Shyan
authors.initials: KS
authors.lastname: Lu
mesh_terms: D000818:Animals; D002460:Cell Line; D051546:Cyclooxygenase 2 / Q000032:analysis; D015232:Dinoprostone / Q000032:analysis; D005227:Fatty Acids / Q000737:chemistry / Q000276:immunology* / Q000494:pharmacology; D005231:Fatty Acids, Unsaturated / Q000737:chemistry / Q000276:immunology* / Q000494:pharmacology; D007249:Inflammation / Q000276:immunology*; D015850:Interleukin-6 / Q000276:immunology; D018950:Lipopolysaccharide Receptors / Q000032:analysis; D008070:Lipopolysaccharides / Q000276:immunology*; D008264:Macrophages / Q000187:drug effects / Q000276:immunology*; D051379:Mice; D016328:NF-kappa B / Q000032:analysis; D009569:Nitric Oxide / Q000032:analysis; D052247:Nitric Oxide Synthase Type II / Q000032:analysis; D012710:Serum Albumin, Bovine / Q000737:chemistry / Q000276:immunology* / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D005227:Fatty Acids; D005231:Fatty Acids, Unsaturated; D015850:Interleukin-6; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D012710:Serum Albumin, Bovine; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D015232:Dinoprostone
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