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

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.