Respiratory epithelial cells release interleukin-8 in response to a thermophilic bacteria that causes hypersensitivity pneumonitis

Exp Lung Res. Apr-May 1999;25(3):217-28. doi: 10.1080/019021499270277.

Abstract

Hypersensitivity pneumonitis (HP) is a granulomatous inflammatory lung disease that is usually triggered by organic antigens. At early time points after inhalation of antigen, neutrophilic inflammation is prominent in the lungs. Interleukin (IL)-8 is a potent chemoattractant for neutrophils and it is known that alveolar macrophages can release IL-8 after exposure to organic antigens. However, the role of respiratory epithelial cells in the production of IL-8 in HP is unknown. We exposed A549 epithelial cells to the thermophilic bacteria Saccharopolyspora rectivirgula (SR), and measured IL-8 release via enzyme-linked immunosorbent assay (ELISA) and IL-8 messenger RNA (mRNA) induction via Northern analysis. We observed a dose- and time-dependent release of IL-8 in response to SR. The maximal release of IL-8 was measured at 24-48 hours after exposure. There was also an increase in release of IL-6 in a time-dependent fashion. SR induced a peak increase in IL-8 mRNA at 12-24 hours. SR also triggered expression of the DNA-binding activity of NF-kappa B, a transcription factor that mediates activation of the IL-8 gene. Both corticosteroids and IL-10 blocked the production of IL-8. The release of IL8 was not mediated through IL-1 beta. These data suggest that SR-induced IL-8 production in airway epithelium may play a role in the initial inflammatory response in HP.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Alveolitis, Extrinsic Allergic / microbiology*
  • Blotting, Northern
  • Cells, Cultured
  • Dexamethasone / pharmacology
  • Enzyme-Linked Immunosorbent Assay
  • Epithelial Cells / drug effects
  • Epithelial Cells / metabolism*
  • Epithelial Cells / microbiology
  • Humans
  • Interleukin-1 / pharmacology
  • Interleukin-10 / pharmacology
  • Interleukin-8 / biosynthesis*
  • Interleukin-8 / genetics
  • NF-kappa B / metabolism
  • Pulmonary Alveoli / drug effects
  • Pulmonary Alveoli / metabolism*
  • Pulmonary Alveoli / microbiology
  • RNA, Messenger / metabolism
  • Saccharopolyspora / physiology*
  • Time Factors
  • Tumor Cells, Cultured

Substances

  • Interleukin-1
  • Interleukin-8
  • NF-kappa B
  • RNA, Messenger
  • Interleukin-10
  • Dexamethasone