title: Molecular mechanisms of lipopolysaccharide induced ICAM-1 expression in A549 cells.
abstract: OBJECTIVE
  Lung intercellular adhesion molecule-1 (ICAM-1) expression is increased by LPS or hyperoxia on type II cells in vivo. The goals of the present study were to determine the mechanisms of ICAM-1 expression in a lung alveolar epithelial cell line (A549) exposed to lipopolysaccharide (LPS).
  
  
  METHODS
  A549 cells, a transformed human cell line with characteristics of alveolar epithelial cells, were used.
  
  
  METHODS
  Cells were exposed to LPS, TNF-alpha, IL-1beta, or media alone for up to 12 h.
  
  
  METHODS
  Northern blot analyses were done to determine mRNA expression of ICAM-1 after exposures. Protein binding to NF-kappaB sequences were determined by gel mobility shift assays and super-shift analysis.
  
  
  RESULTS
  ICAM-1 mRNA expression was induced in A549 cells with exposure to LPS for 1 to 4 h, and was diminished to baseline at 8 h, and the inductions were independent of TNF-alpha and IL-1beta expression. Nuclear protein extracts from LPS-exposed cells bound to a NF-kappaB sequence and the timing of increased binding correlated closely with ICAM-1 mRNA induction. Super-shift studies indicated that p65 was involved in the binding to the NF-kappaB sequence and p50 was not.
  
  
  CONCLUSIONS
  LPS inducibility of ICAM-1 mRNA in A549 cells is independent of TNF- and IL-1 in A549 cells, and the similar time course of mRNA induction and NF-kappaB activation suggest the induction of ICAM-1 is mediated, in part, by NF-kappaB.
authors.affiliation: Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030, USA. cfakler@neo.bcm.tmc.edu
authors.forename: C R
authors.initials: CR
authors.lastname: Fakler
authors.forename: B
authors.initials: B
authors.lastname: Wu
authors.forename: H W
authors.initials: HW
authors.lastname: McMicken
authors.forename: R S
authors.initials: RS
authors.lastname: Geske
authors.forename: S E
authors.initials: SE
authors.lastname: Welty
mesh_terms: D001665:Binding Sites; D015152:Blotting, Northern; D002461:Cell Line, Transformed; D004847:Epithelial Cells / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics*; D007375:Interleukin-1 / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology*; D016328:NF-kappa B / Q000378:metabolism; D011650:Pulmonary Alveoli / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D007375:Interleukin-1; D008070:Lipopolysaccharides; D016328:NF-kappa B; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1