Acute systemic inflammation transiently synchronizes clock gene expression in equine peripheral blood
| Autor: | Barbara A. Murphy, Mandi M. Vick, R. Frank Cook, B. P. Fitzgerald, D. R. Sessions |
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| Rok vydání: | 2007 |
| Předmět: |
Lipopolysaccharides
Immunology Circadian clock Inflammation Biology Peripheral blood mononuclear cell Body Temperature Behavioral Neuroscience Immune system Biological Clocks Oscillometry Basic Helix-Loop-Helix Transcription Factors medicine Animals Horses Analysis of Variance Innate immune system Tumor Necrosis Factor-alpha Endocrine and Autonomic Systems Suprachiasmatic nucleus ARNTL Transcription Factors Nuclear Proteins Adaptation Physiological Circadian Rhythm CLOCK PER2 Gene Expression Regulation Female medicine.symptom Transcription Factors |
| Zdroj: | Brain, Behavior, and Immunity. 21:467-476 |
| ISSN: | 0889-1591 |
| DOI: | 10.1016/j.bbi.2006.11.002 |
| Popis: | Peripheral clocks receive timing signals from the master mammalian pacemaker in the suprachiasmatic nucleus (SCN) and function to adaptively anticipate daily changes that influence local physiology. Evidence suggests that peripheral immune activation may act as a resetting signal for circadian clocks in peripheral tissues. We wished to investigate whether acute systemic inflammation could synchronize clock gene expression in equine peripheral blood, a tissue that does not normally oscillate in this species. We report that in vivo administration of lipopolysaccharide (LPS) results in significant upregulation of the core clock genes Per2 and Bmal1 in equine blood, in association with an acute rise in tumor necrosis factor (TNF) alpha and core body temperature compared to vehicle-treated control animals. Furthermore, co-administration of LPS and phenylbutazone, a non-steroidal anti-inflammatory drug (NSAID) known to inhibit prostaglandin (PG) E(2) synthesis in the horse, prevents both the febrile response and the synchronized increase in clock gene expression. However, the rise in Per2 and Bmal1 expression cannot be replicated in equine peripheral blood mononuclear cells (PBMCs) ex vivo by treatment with PGE(2), LPS or a heat shock mimicking the in vivo febrile response. These results may suggest an indirect communication pathway between immune modulators and the molecular machinery of cell clocks in peripheral blood. This potential immune feedback regulation of an equine peripheral clock implies a role for the circadian system in contributing to innate immune reactions and maintaining homeostasis in a tissue that acts as the first line of defense during an infectious challenge. |
| Databáze: | OpenAIRE |
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