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

C. Porta, V. Rizzo, M. Zimatore, A. Sartore-Bianchi, M. Danova, L. Mutti

Research output: Contribution to journalArticle

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.

Original languageEnglish
Pages (from-to)159-162
Number of pages4
JournalLung Cancer
Volume38
Issue number2
DOIs
Publication statusPublished - Nov 1 2002

Keywords

  • Cytotoxicity
  • Intrapleural IL-2
  • Malignant mesothelioma
  • Nitric oxide

ASJC Scopus subject areas

  • Oncology

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