Adaptation to bacterial lipopolysaccharide controls lipopolysaccharide-induced tumor necrosis factor production in rabbit macrophages
| Autor: | John C. Mathison, E Wolfson, Richard J. Ulevitch, Peter S. Tobias, G D Virca, Keith B. Glaser |
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| Rok vydání: | 1990 |
| Předmět: |
Lipopolysaccharides
Staphylococcus aureus medicine.medical_specialty Lipopolysaccharide Indomethacin medicine.disease_cause chemistry.chemical_compound Tumor necrosis factor production Internal medicine medicine Animals Macrophage RNA Messenger Messenger RNA Lagomorpha Dose-Response Relationship Drug biology Tumor Necrosis Factor-alpha Macrophages Interleukin Stereoisomerism General Medicine biology.organism_classification Adaptation Physiological Endocrinology chemistry lipids (amino acids peptides and proteins) Tumor necrosis factor alpha Rabbits Research Article Interleukin-1 |
| Zdroj: | Journal of Clinical Investigation. 85:1108-1118 |
| ISSN: | 0021-9738 |
| DOI: | 10.1172/jci114542 |
| Popis: | These experiments provide an explanation for the observation that two intravenous injections of lipopolysaccharide (LPS) spaced 5 h apart in rabbits cause tumor necrosis factor/cachectin (TNF) levels to rise in the blood only after the first LPS injection. Herein we show that treatment of elicited peritoneal exudate rabbit macrophages (PEM) with two doses of LPS given 9 h apart results in a marked reduction in TNF production by the second LPS exposure. This state of hyporesponsiveness is a result of adaptation to LPS, is induced by LPS concentrations that are 1,000-fold less than required to induce TNF production (picograms vs. nanograms), is characterized by a decrease in LPS-induced TNF mRNA without any change in TNF mRNA half-life, is not changed by including indomethacin in cultures, and is specific for LPS since LPS-adapted cells display a TNF response to heat-killed Staphylococcus aureus that is at least as good as that observed in control PEM. |
| Databáze: | OpenAIRE |
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