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Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on November 10, 2003; DOI: 10.1124/jpet.103.058198

0022-3565/04/3082-754-759$20.00
JPET 308:754-759, 2004
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INFLAMMATION AND IMMUNOPHARMACOLOGY

Granulocyte Colony-Stimulating Factor (Filgrastim) Treatment Primes for Increased ex Vivo Inducible Prostanoid Release

Sonja von Aulock, Eva-Maria Boneberg, Isabel Diterich, and Thomas Hartung

Biochemical Pharmacology, University of Konstanz, Konstanz, Germany

We investigated whether anti-inflammatory effects of treatment with granulocyte colony-stimulating factor (G-CSF, filgrastim) are mediated via prostaglandin E2 (PGE2) induction. In a double-blind crossover study, 10 healthy volunteers received 300 µg of filgrastim or saline 1 week apart. This was repeated after oral administration of 50 mg of flurbiprofen 1 h before injection. The increase in neutrophilic granulocytes initiated by G-CSF was augmented significantly by flurbiprofen. Lipopolysaccharide-induced PGE2 and thromboxane (TxB2) release were increased 8 h after G-CSF treatment. This increase was abrogated by flurbiprofen. However, flurbiprofen did not affect G-CSF-mediated decrease in tumor necrosis factor-{alpha} or interferon-{gamma} release. Of the volunteers treated with G-CSF, eight reported side effects (headache and bone pain) against none in the saline group. When flurbiprofen was given before injection, one volunteer each reported side effects in the G-CSF and in the saline group. These data show that G-CSF primes for increased PGE2 and TxB2 release. Cyclooxygenase inhibition counteracts neither the hematopoietic nor the anti-inflammatory activity of G-CSF but reduces side effects.

Received August 5, 2003; accepted November 7, 2003.

Address correspondence to: Dr. Thomas Hartung, Biochemical Pharmacology, University of Konstanz, P.O. Box M655, 78457 Konstanz, Germany. E-mail: thomas.hartung{at}uni-konstanz.de






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