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• W1984825068 abstract "BackgroundIsocyanates are low-molecular-weight compounds noted for inducing occupational and environmental asthma. Isocyanate-induced lung disease, an oxidant stress-dependent pulmonary inflammation, is the leading cause of occupational asthma.ObjectivesTo address the role of leukocyte-produced oxidants in airway inflammation induced by toluene diisocyanate (TDI), and to elucidate the role of leukocyte nicotinamide adenine dinucleotide phosphate-reduced (NADPH) oxidase in pathogenesis by TDI.MethodsWild-type mice and NADPH oxidase–deficient mice (neutrophil cytosolic factor 1 mutant, Ncf1–/–) were intranasally injected, challenged with inhalatory TDI, and then investigated for lung inflammation.ResultsCell infiltration in lung tissue and leukocytes in bronchoalveolar lavage, airway reactivity to a methacholine challenge, and TDI-induced inflammatory cytokine expression and nuclear factor activation in the lung tissue were all markedly lower in Ncf1–/– mice. Wild-type mice treated with blocking antibodies against CD4 and IL-17 showed markedly lower TDI-induced airway hyperresponsiveness.ConclusionLeukocyte NADPH oxidase is an essential regulator in TDI-induced airway inflammation through redox modification of immune responses. Isocyanates are low-molecular-weight compounds noted for inducing occupational and environmental asthma. Isocyanate-induced lung disease, an oxidant stress-dependent pulmonary inflammation, is the leading cause of occupational asthma. To address the role of leukocyte-produced oxidants in airway inflammation induced by toluene diisocyanate (TDI), and to elucidate the role of leukocyte nicotinamide adenine dinucleotide phosphate-reduced (NADPH) oxidase in pathogenesis by TDI. Wild-type mice and NADPH oxidase–deficient mice (neutrophil cytosolic factor 1 mutant, Ncf1–/–) were intranasally injected, challenged with inhalatory TDI, and then investigated for lung inflammation. Cell infiltration in lung tissue and leukocytes in bronchoalveolar lavage, airway reactivity to a methacholine challenge, and TDI-induced inflammatory cytokine expression and nuclear factor activation in the lung tissue were all markedly lower in Ncf1–/– mice. Wild-type mice treated with blocking antibodies against CD4 and IL-17 showed markedly lower TDI-induced airway hyperresponsiveness. Leukocyte NADPH oxidase is an essential regulator in TDI-induced airway inflammation through redox modification of immune responses." @default.
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• W1984825068 date "2011-04-01" @default.
• W1984825068 modified "2023-10-16" @default.
• W1984825068 title "Leukocyte nicotinamide adenine dinucleotide phosphate-reduced oxidase is required for isocyanate-induced lung inflammation" @default.
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• W1984825068 doi "https://doi.org/10.1016/j.jaci.2010.12.008" @default.
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