title: Soot-exposed mononuclear cells increase inflammatory cytokine mRNA expression and protein secretion in cocultured bronchial epithelial cells.
abstract: BACKGROUND
  Soot particles are air pollutants capable of inducing airway and lung parenchymal injury. Mononuclear and bronchial epithelial cells are central to the maintenance of homeostasis and inflammation in the airways.
  
  
  OBJECTIVE
  The aim of this study was to evaluate the contribution of mononuclear cells to the release of inflammatory mediators by bronchial epithelial cells.
  
  
  METHODS
  To model the in vivo situation, an in vitro system of cocultured blood monocytes and BEAS-2B cells was established in a transwell system. Blood monocytes were exposed to soot particles (FR 101) at concentrations of up to 100 microg/10(6) cells. Inflammatory cytokine mRNA and protein concentrations were quantified in BEAS-2B mono- and BEAS-2B-BM cocultures by RT-PCR and ELISA following exposure to soot for 1 and 8 h.
  
  
  RESULTS
  No inflammatory cytokine mRNA expression was observed in unstimulated BEAS-2B cells. IL-6 and IL-8 mRNA and protein levels showed a dose-dependent elevation in FR 101-exposed blood monocytes. In addition, both IL-6 and IL-8 mRNA expression was upregulated in cocultured BEAS-2B cells while cytokine concentrations in the blood monocyte-BEAS-2B coculture medium were significantly increased. This upregulation was likely due to a synergism of two cell populations.
  
  
  CONCLUSIONS
  Exposure to soot particles induces an autocrine stimulation of inflammatory cytokine release by blood monocytes and BEAS-2B cells. Since IL-6 and IL-8 play a major role in the pathogenesis and persistence of bronchial inflammation, these findings may serve as a partial explanation for the aggravation of asthmatic and bronchitic symptoms after exposure to soot.
authors.affiliation: Pulmonary Division, Third Medical Department, Johannes Gutenberg University, Mainz, Germany.
authors.forename: K
authors.initials: K
authors.lastname: Drumm
authors.forename: D I
authors.initials: DI
authors.lastname: Attia
authors.forename: S
authors.initials: S
authors.lastname: Kannt
authors.forename: P
authors.initials: P
authors.lastname: Micke
authors.forename: R
authors.initials: R
authors.lastname: Buhl
authors.forename: K
authors.initials: K
authors.lastname: Kienast
mesh_terms: D000328:Adult; D000393:Air Pollutants / Q000009:adverse effects*; D001798:Blood Proteins / Q000378:metabolism*; D001980:Bronchi / Q000166:cytology / Q000276:immunology*; D002244:Carbon / Q000009:adverse effects*; D002478:Cells, Cultured; D018920:Coculture Techniques; D016207:Cytokines / Q000032:analysis / Q000235:genetics; D004797:Enzyme-Linked Immunosorbent Assay; D004847:Epithelial Cells / Q000378:metabolism*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis*; D015850:Interleukin-6 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D008297:Male; D009000:Monocytes / Q000276:immunology*; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012680:Sensitivity and Specificity
chemical_list: D000393:Air Pollutants; D001798:Blood Proteins; D016207:Cytokines; D018836:Inflammation Mediators; D015850:Interleukin-6; D016209:Interleukin-8; D012333:RNA, Messenger; D002244:Carbon