Cyclic AMP increases endogenous granulocyte colony-stimulating factor formation in monocytes and THP-1 macrophages despite attenuated TNF-alpha formation

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2003
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European Journal of Immunology. 2003, 33(8), pp. 2287-2296. ISSN 0014-2980. eISSN 1521-4141. Available under: doi: 10.1002/eji.200323923
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The cytokine granulocyte colony-stimulating factor (G-CSF) is in broad clinical use to treat neutropenia, and trials on its use in immunosuppressed conditions and infections are ongoing. To aply G-CSF effectively, it is crucial to understand the regulation and distribution of its endogenous formation. Since G-CSF release is mediated, at least in part, by TNF-α formation, we investigated whether drugs suppressing TNF-α also impair G-CSF production. Surprisingly, G-CSF formation was enhanced in lipopolysaccharide (LPS)-stimulated blood from a pentoxifylline-treated patient. In the presence of dibutyryl-cAMP, forskolin, tolafentrine or 3-isobutyl-1-methylxanthine, LPS-induced G-CSF formation was enhanced in THP-1 cells, primary monocytes and whole blood. Correspondingly,rp-8-bromo-cAMP suppressed LPS-induced G-CSF release. Addition of prostaglandin E2 enhanced and indomethacin suppressed G-CSF formation. Reporter gene studies showed that dibutyryl-cAMP enhanced LPS-induced G-CSF promoter activity, indicating a transcriptional up-regulation. Furthermore, disruption of a newly identified putative cAMP-responsive element (CRE) in the G-CSF promoter demonstrated the regulatory role for G-CSF gene transcription. In conclusion, endogenous G-CSF formation critically depends on both TNF-α and cyclooxygenase products, exerting effects via cAMP and the CREin the G-CSF promoter. This might have bearing for drug side effects, putative G-CSF mimetics and our understanding of G-CSF immunobiology.

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570 Biowissenschaften, Biologie
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Granulocyte colony-stimulating factor, cAMP-responsive element, TNF-alpha, Prostaglandin E2, Monocyte
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ISO 690HARENG, Lars, Thomas MEERGANS, Sonja von AULOCK, Hans-Dieter VOLK, Thomas HARTUNG, 2003. Cyclic AMP increases endogenous granulocyte colony-stimulating factor formation in monocytes and THP-1 macrophages despite attenuated TNF-alpha formation. In: European Journal of Immunology. 2003, 33(8), pp. 2287-2296. ISSN 0014-2980. eISSN 1521-4141. Available under: doi: 10.1002/eji.200323923
BibTex
@article{Hareng2003Cycli-1230,
  year={2003},
  doi={10.1002/eji.200323923},
  title={Cyclic AMP increases endogenous granulocyte colony-stimulating factor formation in monocytes and THP-1 macrophages despite attenuated TNF-alpha formation},
  number={8},
  volume={33},
  issn={0014-2980},
  journal={European Journal of Immunology},
  pages={2287--2296},
  author={Hareng, Lars and Meergans, Thomas and Aulock, Sonja von and Volk, Hans-Dieter and Hartung, Thomas}
}
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    <dcterms:abstract xml:lang="eng">The cytokine granulocyte colony-stimulating factor (G-CSF) is in broad clinical use to treat neutropenia, and trials on its use in immunosuppressed conditions and infections are ongoing. To aply G-CSF effectively, it is crucial to understand the regulation and distribution of its endogenous formation. Since G-CSF release is mediated, at least in part, by TNF-α formation, we investigated whether drugs suppressing TNF-α also impair G-CSF production. Surprisingly, G-CSF formation was enhanced in lipopolysaccharide (LPS)-stimulated blood from a pentoxifylline-treated patient. In the presence of dibutyryl-cAMP, forskolin, tolafentrine or 3-isobutyl-1-methylxanthine, LPS-induced G-CSF formation was enhanced in THP-1 cells, primary monocytes and whole blood. Correspondingly,rp-8-bromo-cAMP suppressed LPS-induced G-CSF release. Addition of prostaglandin E2 enhanced and indomethacin suppressed G-CSF formation. Reporter gene studies showed that dibutyryl-cAMP enhanced LPS-induced G-CSF promoter activity, indicating a transcriptional up-regulation. Furthermore, disruption of a newly identified putative cAMP-responsive element (CRE) in the G-CSF promoter demonstrated the regulatory role for G-CSF gene transcription. In conclusion, endogenous G-CSF formation critically depends on both TNF-α and cyclooxygenase products, exerting effects via cAMP and the CREin the G-CSF promoter. This might have bearing for drug side effects, putative G-CSF mimetics and our understanding of G-CSF immunobiology.</dcterms:abstract>
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