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SHR Neuro Cancer Cardio Lipid Metab Microb
Ulcar, R; Peskar, BA; Schuligoi, R; Heinemann, A; Kessler, HH; Santner, BI; Amann, R.
Cyclooxygenase inhibition in human monocytes increases endotoxin-induced TNF alpha without affecting cyclooxygenase-2 expression.
EUR J PHARMACOL. 2004; 501(1-3): 9-17.
Doi: 10.1016/j.ejphar.2004.08.003
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- Leading authors Med Uni Graz
- Amann Rainer
- Co-authors Med Uni Graz
- Heinemann Akos
- Kessler Harald
- Peskar Bernhard
- Santner Brigitte
- Schuligoi Rufina
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- Abstract:
- Human endotoxin-stimulated adherent monocytes were used in order to determine whether or not NSAIDs influence cyclooxygenase-2 and/or tumor necrosis factor (TNF)alpha expression within the range of inhibitor concentrations that are required to suppress prostaglandin biosynthesis. Exogenous prostaglandin E(2) (IC(50)<5 nM) inhibited endotoxin-induced TNFalpha mRNA and protein while, up to 1 microM, it did not significantly affect cyclooxygenase-2 mRNA expression. Similar results were obtained using the membrane-permeable cAMP analogue db-cAMP, which caused preferential inhibition of TNFalpha expression. Indomethacin or lysine-acetylsalicylic acid concentration-dependently inhibited prostaglandin E(2) biosynthesis and, at concentrations causing near-complete inhibition, enhanced TNFalpha mRNA and protein expression without significantly influencing cyclooxygenase-2 mRNA. In addition, by facilitating endotoxin-induced TNFalpha expression, indomethacin or lysine-acetylsalicylic acid counteracted dexamethasone-induced inhibition of TNFalpha biosynthesis, thereby exhibiting an effect opposite to that of exogenous prostaglandin E(2). The results suggest that in human endotoxin-stimulated monocytes, NSAIDs can enhance TNFalpha expression through inhibition of cyclooxygenase and the resulting decrease in prostanoid biosynthesis.
- Find related publications in this database (using NLM MeSH Indexing)
- Cells, Cultured -
- Cyclooxygenase 2 -
- Cyclooxygenase 2 Inhibitors -
- Cyclooxygenase Inhibitors - pharmacology
- Dose-Response Relationship, Drug - pharmacology
- Endotoxins - pharmacology
- Gene Expression Regulation, Enzymologic - drug effects
- Humans - drug effects
- Membrane Proteins - drug effects
- Monocytes - drug effects
- Prostaglandin-Endoperoxide Synthases - biosynthesis
- Tumor Necrosis Factor-alpha - biosynthesis
- Find related publications in this database (Keywords)
- NSAID
- prostaglandin E-2
- TNF alpha
- cyclooxygenase
- glucocorticoid
- monocyte
- human