The anti-inflammatory cytokine interleukin (IL)-10 suppresses inducible nitric oxide synthase (iNOS); therefore, NO production should increase in the absence of IL-10. Production of NO (as nitrite) by bronchoalveolar lavage cells of IL-10 knockout (-/-) mice was assessed after ovalbumin sensitization and airway challenge (S/C) and was compared with the IL-10-sufficient, wild-type (WT) C57B6. Eosinophil recruitment occurred in S/C WT and IL-10-/- mice, suggesting allergic airway inflammation. Alveolar macrophages (per g mouse) were unchanged (∼3×104 cells) with the exception of a doubling in the S/C IL-10-/- mice (∼6×104 cells, P<0.05). NO production (per million cells) was doubled in cells from S/C IL-10-/- (15.3 μM) mice compared with WT (7.6 μM, P<0.05). Inhibition of iNOS by L-N5-(l-iminoethyl)-ornithine reduced NO production in all S/C mice, confirming that the increase was a result of up-regulation of iNOS. We conclude that IL-10 is a critical cytokine regulating iNOS in murine airway cells and that its absence can lead to up-regulation of iNOS and development of allergic airway inflammation.
|Number of pages||7|
|Journal||Journal of Leukocyte Biology|
|State||Published - 2001|
- Bronchoalveolar lavage
- C57BL6 mice