Due to the frequent use of intrapleural interleukin-2 (IL-2) to treat pleural effusions from malignant mesothelioma (MMe), we measured nitric oxide (NO) end product nitrite (NO2-) in pleural effusions of 12 MMe patients with chronic or chronic-relapsing pleurisy. Through high performance liquid chromatography analysis, NO2- was found in the initial pleural fluid sample of all patients (156.25 pmolml-1), and increased significantly following IL-2 intrapleural instillation, both at 24 (589.91 pmolml-1, P≤0.0005) and 48 h (756 pmolml-1, P≤0.0005). Even though it is difficult to argue if the large amounts of NO end product NO2- we observed is produced by IL-2-stimulated and recruited immune cells, by MMe cells themselves, or by both, it is possible that NO could contribute to the complex antitumor activity of IL-2. © 2002 Elsevier Science Ireland Ltd.

Intrapleural interleukin-2 induces nitric oxide production in pleural effusions from malignant mesothelioma: A possible mechanism of interleukin-2-mediated cytotoxicity?

Mutti L.
2002-01-01

Abstract

Due to the frequent use of intrapleural interleukin-2 (IL-2) to treat pleural effusions from malignant mesothelioma (MMe), we measured nitric oxide (NO) end product nitrite (NO2-) in pleural effusions of 12 MMe patients with chronic or chronic-relapsing pleurisy. Through high performance liquid chromatography analysis, NO2- was found in the initial pleural fluid sample of all patients (156.25 pmolml-1), and increased significantly following IL-2 intrapleural instillation, both at 24 (589.91 pmolml-1, P≤0.0005) and 48 h (756 pmolml-1, P≤0.0005). Even though it is difficult to argue if the large amounts of NO end product NO2- we observed is produced by IL-2-stimulated and recruited immune cells, by MMe cells themselves, or by both, it is possible that NO could contribute to the complex antitumor activity of IL-2. © 2002 Elsevier Science Ireland Ltd.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11697/222932
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