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Published on: July 24, 2018
Acute systemic inflammation transiently synchronizes clock gene expression in equine peripheral blood
Barbara A Murphy1, Mandi M Vick, Dawn R Sessions
1Maxwell H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, KY 40546-0099, USA. babsmurphy@gmail.com
Brain, Behavior, and Immunity
|December 19, 2006
Summary
Acute systemic inflammation synchronizes equine peripheral clock gene expression via an indirect pathway. Lipopolysaccharide (LPS) increased clock genes Per2 and Bmal1, an effect blocked by phenylbutazone.
Area of Science:
- Circadian biology
- Immunology
- Equine physiology
Background:
- Peripheral circadian clocks anticipate daily physiological changes.
- Immune activation may reset peripheral circadian clocks.
- Equine peripheral blood typically lacks circadian oscillation.
Purpose of the Study:
- To investigate if acute systemic inflammation synchronizes clock gene expression in equine peripheral blood.
- To explore the role of inflammation in regulating peripheral circadian rhythms in horses.
Main Methods:
- In vivo administration of lipopolysaccharide (LPS) to horses.
- Measurement of core clock genes (Per2, Bmal1), tumor necrosis factor (TNF) alpha, and core body temperature.
- Co-administration of LPS with phenylbutazone (NSAID) to assess prostaglandin (PG) E(2) inhibition.
- Ex vivo treatment of equine peripheral blood mononuclear cells (PBMCs) with PGE(2), LPS, or heat shock.
Main Results:
- LPS administration upregulated Per2 and Bmal1 expression in equine blood, accompanied by increased TNF alpha and body temperature.
- Phenylbutazone blocked the febrile response and synchronized clock gene expression.
- Ex vivo treatments (PGE(2), LPS, heat shock) did not replicate the in vivo clock gene upregulation in PBMCs.
- Results suggest an indirect communication pathway between immune modulators and peripheral cell clocks.
Conclusions:
- Acute systemic inflammation can synchronize clock gene expression in equine peripheral blood, suggesting immune-mediated regulation of peripheral circadian clocks.
- The mechanism appears indirect, possibly involving signaling molecules other than PGE(2) acting directly on PBMCs.
- This immune feedback regulation highlights the circadian system's role in innate immunity and homeostasis during infection.
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