Respiratory epithelial cells release interleukin-8 in response to a thermophilic bacteria that causes hypersensitivity pneumonitis.
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.[1]References
- Respiratory epithelial cells release interleukin-8 in response to a thermophilic bacteria that causes hypersensitivity pneumonitis. Gudmundsson, G., Hunninghake, G.W. Exp. Lung Res. (1999) [Pubmed]
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