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* Asthma, Allergy, and Airway Research Center, Division of Pulmonary, Allergy, and Critical Care Medicine,
Department of Surgery, and
Department of Cell Biology and Physiology, University of Pittsburgh School of Medicine, Pennsylvania
Correspondence: Bill T. Ameredes, Ph.D., Assistant Professor of Cell Biology and Physiology, Asthma, Allergy, and Airway Research Center, Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh School of Medicine, 628NW Montefiore University Hospital, 3459 Fifth Ave., Pittsburgh, PA 15213. E-mail: ameredesbt{at}msx.upmc.edu
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) C57Bl6.
Eosinophil recruitment occurred in S/C WT and IL-10-/-
mice, suggesting allergic airway inflammation. Alveolar macrophages
(per g mouse) were unchanged (
3x104 cells) with the
exception of a doubling in the S/C IL-10-/- mice
(6x104 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-(1-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.
Key Words: allergen • bronchoalveolar lavage • C57BL6 mice • macrophage • nitrite • ovalbumin
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