Nitric Oxide Blocks Nuclear Factor- κ B Activation in Alveolar Macrophages

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Abstract
Nitric oxide (NO) is an important endogenous regulatory molecule implicated in both proinflammatory and antiinflammatory processes in the lung. Previously, we demonstrated that in human alveolar macrophages (AM), NO decreased inflammatory cytokine production, including that of interleukin-1β, tumor necrosis factor-α and macrophage inflammatory protein-1α. One mechanism by which NO could regulate such diverse cytokine production is through effects on the transcription factor nuclear factor-κB (NF-κB), which controls the expression of the genes for these inflammatory cytokines and growth factors. We therefore investigated whether NO affects NF-κB activation in AM in vitro and in vivo. In vitro studies with AM showed that NF-κB activation by lipopolysaccharide (LPS) is decreased by NO in a dose-dependent manner. NO prevented an LPS-mediated decrease in the NF-κB inhibitory protein IκB-α. In asthma, airway NO levels are increased, whereas in primary pulmonary hypertension (PPH), airway NO levels are lower tha...

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