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Alterations in Nitric Oxide and Cytokine Production with Airway Inflammation in the Absence of IL-10¹

Bill T. Ameredes^2,*,, Ruben Zamora, Jigme M. Sethi, He-Liang Liu^*,, Lauryn K. Kohut^*,, Amber L. Gligonic^*,, Augustine M. K. Choi and William J. Calhoun^*,

^* Asthma, Allergy, and Airway Research Center, Division of Pulmonary, Allergy, and Critical Care Medicine, and Department of Surgery, University of Pittsburgh School of Medicine Pittsburgh, PA 15261

IL-10 is an anti-inflammatory cytokine that suppresses NO synthase (NOS) and production of NO; its lack may promote NO production and alterations in cytokines modulated by NO with allergic airway inflammation (AI), such as IL-18 and IL-4. Therefore, we induced AI in IL-10 knockout (^–/–) and IL-10-sufficient C57BL/6 (C57) mice with inhaled OVA and measured airway NO production, as exhaled NO (E_NO) and bronchoalveolar lavage fluid nitrite levels. E_NO and nitrite levels were elevated significantly in naive IL-10^–/– mice as compared with C57 mice. With AI, E_NO and nitrite levels increased in C57 mice and decreased in IL-10^–/– mice. IL-18 production fell with both AI and addition of S-nitroso-N-acetyl-D,L-penicillamine (a NO donor) but was not significantly increased by chemical NOS inhibition by L-N⁵-(1-iminoethyl)-ornithine. IL-4 AI was increased significantly (up to 10-fold greater) in the absence of IL-10 but was reduced significantly with chemical inhibition of NOS. Airway responsiveness was lower in IL-10^–/– mice and was associated with alteration in production of NO and IL-4. Thus, IL-4 production was increased, and likely decreased NO production, in a way not predicted by the absence of IL-10. Inhibition of IL-4 production, with inhibition of NOS in the absence of IL-10, demonstrated the importance of a NO and IL-4 feedback mechanism regulating this interaction.

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