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The inflammatory cytokines tumor necrosis factor α and interleukin-1β stimulate phosphatidylcholine secretion in primary cultures of rat type II pneumocytes

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Abstract

Tumor necrosis factor α and interleukin-1β increase surfactant secretion in type II pneumocytes in a time- and dose-dependent manner. This stimulatory effect was additive to that of lipopolysaccharide, suggesting that cytokines and lipopolysaccharide may exert their actions through different signal transduction pathways. Tumor necrosis factor α and interleukin-1β did not modify the increase on phosphatidylcholine secretion induced by the direct protein kinase C activator tetradecanoylphorbol 13-acetate, whereas this effect was inhibited by the protein kinase C inhibitors bisindolylmaleimide (2 × 10-6M) and 1-(5-isoquinolinylsulphonyl)-2-methyl piperazone (10-4M). In addition, the stimulatory effect of tumor necrosis factor α and interleukin-1β was not suppressed by the intracellular Ca2+ chelator BAPTA (5 × 10-6M) or by KN-62 (3 × 10-5M), a specific inhibitor of Ca2+-calmodulin-dependent protein kinase. These results suggest that tumor necrosis factor α or interleukin-1β stimulate phosphatidylcholine secretion via protein kinase C activation in a Ca2+ -independent manner.

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Authors and Affiliations

  1. Department of Biochemistry and Molecular Biology, Faculty of Chemistry, Universidad Complutense, Madrid, Spain

    Enrique Benito & María A. Bosch

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  1. Enrique Benito
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  2. María A. Bosch
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Benito, E., Bosch, M.A. The inflammatory cytokines tumor necrosis factor α and interleukin-1β stimulate phosphatidylcholine secretion in primary cultures of rat type II pneumocytes. Mol Cell Biochem 189, 169–176 (1998). https://doi.org/10.1023/A:1006997731607

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