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- W1967541128 abstract "We tested the hypothesis that NO synthase inhibition alters proinflammatory cytokine expression during acute lung injury in mice. Five-week-old CD-1 mice were pretreated with l-NAME or d-NAME and then received an intratracheal injection of endotoxin (or PBS). TNF- α and IL-6 ELISAs and RT-PCR were performed on lung homogenates sampled 6 h later. l-NAME increased TNF- α and IL-6 protein and mRNA expression in lungs. Immunostaining demonstrated that TNF- α was expressed predominantly by macrophages in the lung. l-NAME did not alter pulmonary macrophage concentration. To better understand the effect of NO synthase inhibition, elicited murine peritoneal macrophages were stimulated in vitro with LPS after addition of l-NAME, d-NAME, nitroprusside, or control. Nuclear proteins were extracted 3 h later and electrophoretic mobility shift and supershift assays were performed using radiolabeled NF- κ B consensus sequence oligonucleotides. Endotoxin increased NF- κ B p50/p65 heterodimer binding. Binding was further increased by l-NAME and decreased by nitroprusside. The effect of nitroprusside was not blocked by guanylate cyclase inhibition. We conclude that, in endotoxin-induced acute lung injury, NO synthase inhibition increases proinflammatory cytokine protein and mRNA expression in part because NO decreases the amount of NF- κ B available for binding to the regulatory region of proinflammatory cytokine genes." @default.
- W1967541128 created "2016-06-24" @default.
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- W1967541128 date "1999-08-01" @default.
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- W1967541128 title "Modulation of Proinflammatory Cytokines by Nitric Oxide in Murine Acute Lung Injury" @default.
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- W1967541128 doi "https://doi.org/10.1164/ajrccm.160.2.9809081" @default.
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