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 Printable version |
Spontaneous and interleukin-2-modulated cytokine release by bronchoalveolar cells in pulmonary malignancy |
European Cytokine Network. Volume 8, Number 4, 395-400, December 1997, Review
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 Free Article
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Author(s) : Karoline I. Gaede, Gernot Zissel, Udo Schwuléra, Wilhelm G. Struff, Joachim Lorenz, Walter E. Aulitzky, Peter Zipfel, Silke Schrum, Max Schlaak, Christoph Huber, Joachim Müller-Quernheim |
Summary : In a recent phase I study of inhalative, human natural interleukin-2 (hnIL-2) treatment of pulmonary metastases from previously resected solid tumors (mainly renal carcinoma), we have reported that this treatment resulted in an increased accessory function of alveolar macrophages (AM) [1]. Encouraged by these data, we investigated the influence of hnIL-2 inhalation on proinflammatory cytokines spontaneously released by AM. Bronchoalveolar lavage was performed in four groups, each of four patients, before and after 2 weeks of daily inhalation of 0, 200,000, 600,000 and 1,200,000 IU of hnIL-2, respectively. Bronchoalveolar cells were cultured without stimulation to allow spontaneous release over a period of 24 h, into the supernatant. Concentrations of tumor necrosis factor-α (TNF-α), IL-6, IL-8 and macrophage inflammatory protein-1α (MIP-1α) were determined by the ELISA technique. Before hnIL-2 inhalation, we measured the following spontaneous cytokine release : TNF-α : 1,115.4 + 469.1 pg/ml, IL-6 : 267.5 + 67.7 pg/ml cells, IL-8 : 137.8 + 40.5 ng/ml, MIP-1α : 9.5 + 6.8 ng/ml. Inhalation of hnIL-2 did not result in any significant changes in these cytokines. Comparing TNF-α release in healthy controls (250.6 ± 46.7 pg/ml) with that of tumor patients (1,115.4 ± 469.1 pg/ml), we observed significantly (p < 0.05) elevated TNF-α levels in the patient group, which did not change significantly in response to IL-2 inhalation. Our data demonstrate that the activation of AM previously observed after hnIL-2 inhalation is not directly related to a hnIL-2-induced cytokine release by bronchoalveolar cells. |
Keywords : IL-2, immunotherapy, bronchoalveolar lavage, neoplasm. |
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