Related Experiment Video
Updated: Jun 17, 2026

Targeted Knockdown of Genes in the Choroid Plexus
Published on: June 16, 2023
Lipopolysaccharide and TNF-alpha modify adenosine A(2A) receptor expression and function in equine monocytes
Wan-chun Sun1, Londa J Berghaus, James N Moore
1Department of Large Animal Medicine, College of Veterinary Medicine, University of Georgia, Athens, GA 30602, United States.
Pro-inflammatory substances like LPS and TNF-alpha increase adenosine A(2A) receptors in horse monocytes. This enhances the anti-inflammatory effects of A(2A) receptor agonists, suggesting their therapeutic potential for equine inflammatory conditions.
Area of Science:
- Immunology
- Pharmacology
Background:
- Adenosine A(2A) receptors exert anti-inflammatory effects.
- Pro-inflammatory stimuli (LPS, TNF-alpha) up-regulate A(2A) receptor expression and function in human and murine monocytes/macrophages.
Purpose of the Study:
- To investigate the effects of LPS and TNF-alpha on adenosine A(2A) receptor expression and function in equine peripheral blood monocytes.
- To assess the potential of A(2A) receptor agonists in treating inflammatory conditions in horses.
Main Methods:
- Isolated equine monocytes were incubated with LPS and TNF-alpha.
- Adenosine A(2A) and A(3) receptor mRNA expression was analyzed.
- Surface density of A(2A) receptors was measured.
- The potency of the A(2A) receptor agonist ATL313 was evaluated in inhibiting LPS-induced TNF-alpha production.
Main Results:
- LPS and TNF-alpha up-regulated adenosine A(2A) receptor transcription for up to 24 hours, with LPS showing a greater effect.
- LPS, but not TNF-alpha, down-regulated adenosine A(3) receptor mRNA expression.
- LPS increased the surface density of adenosine A(2A) receptors.
- Low concentrations of LPS or TNF-alpha enhanced the potency of the A(2A) receptor agonist ATL313 in inhibiting TNF-alpha production.
Conclusions:
- Pro-inflammatory substances increase adenosine A(2A) receptor expression and functional potency in equine monocytes.
- Adenosine A(2A) receptor agonists may be valuable therapeutic agents for treating inflammatory conditions like endotoxemia and bacterial infections in horses.
More Related Videos
11:48Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes
Published on: May 31, 2018
11:29HPLC-based Assay to Monitor Extracellular Nucleotide/Nucleoside Metabolism in Human Chronic Lymphocytic Leukemia Cells
Published on: July 20, 2016
Related Concept Videos
Adrenergic Receptors: ɑ Subtype
Adrenaline ≥ Noradrenaline >> Isoprenaline
α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
α1-Adrenoceptors: These receptors are located postsynaptically on the effector organs and cause constriction of smooth muscle mediated by activation of phospholipase C—inositol-1,4,5-trisphosphate...
Adrenergic Receptors: β Subtype
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors have equal affinities for...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
Adrenergic Antagonists: ɑ and β-Receptor Blockers
GPCRs Regulate Adenylyl Cylase Activity
Two...
Adrenergic Receptors (Adrenoceptors): Classification
α-Adrenoceptors
α-Adrenoceptors are classified into two main subtypes: α1 and α2. The α1 adrenoceptors, which are found on postsynaptic...