title: Perfluorocarbon blocks tumor necrosis factor-alpha-induced interleukin-8 release from alveolar epithelial cells in vitro.
abstract: OBJECTIVE
  To determine whether tumor necrosis factor (TNF)-alpha-induced interleukin (IL)-8 production by pulmonary alveolar epithelial cells is blocked by perfluorocarbon (PFC).
  
  
  METHODS
  Controlled, laboratory investigation of IL-8 production by pulmonary alveolar epithelial cells after exposure to PFC in vitro.
  
  
  METHODS
  University research laboratory.
  
  
  METHODS
  The human alveolar epithelial cell line with pulmonary type II (A549) cell properties.
  
  
  METHODS
  The A549 cells on a polycarbonate porous filter were stimulated either on the apical or the basolateral side with TNF-alpha. To determine TNF-alpha-induced IL-8 production, IL-8 was measured by using a human IL-8 kit in both control and experimental groups.
  
  
  RESULTS
  TNF-alpha stimulation induced a large increase in IL-8. When PFC was added to the medium immediately after TNF-alpha stimulation, PFC separated the medium from the cells and IL-8 production was markedly reduced (TNF-alpha alone, 8342+/-470 pg vs. TNF-alpha followed by PFC, 417+/-88 pg, p < .05). Preincubation of A549 cells with PFC for 24 hrs before stimulation with TNF-alpha followed by removal of PFC did not affect IL-8 production (8834+/-204 vs. 8342+/-470 pg; p = NS). When added to the lower chamber, TNF-alpha also induced IL-8 production unaffected by the addition of PFC to the upper chamber. The decrease in TNF-alpha-induced IL-8 production depended on the time of PFC administration after the initiation of TNF-alpha stimulation. The earlier PFC was added, the more pronounced the diminution was in IL-8.
  
  
  CONCLUSIONS
  PFC appears to function as a physical barrier, thus reducing cytokines produced by alveolar epithelial cells in vitro. This mechanism may partially explain the decreased inflammatory response observed during liquid ventilation in models of acute lung injury.
authors.affiliation: Department of Medicine, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.
authors.forename: A
authors.initials: A
authors.lastname: Baba
authors.forename: Y K
authors.initials: YK
authors.lastname: Kim
authors.forename: H
authors.initials: H
authors.lastname: Zhang
authors.forename: M
authors.initials: M
authors.lastname: Liu
authors.forename: A S
authors.initials: AS
authors.lastname: Slutsky
mesh_terms: D002282:Adenocarcinoma, Bronchiolo-Alveolar; D002450:Cell Communication / Q000187:drug effects; D004347:Drug Interactions; D004847:Epithelial Cells / Q000187:drug effects* / Q000502:physiology; D005466:Fluorocarbons / Q000494:pharmacology*; D006801:Humans; D016209:Interleukin-8 / Q000096:biosynthesis*; D008175:Lung Neoplasms; D011650:Pulmonary Alveoli / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D013997:Time Factors; D014407:Tumor Cells, Cultured; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000187:drug effects
chemical_list: D005466:Fluorocarbons; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha