Abstract
Recent evidence has shown that eosinophils play an important role in metabolic homeostasis through Th2 cytokine production. GPR120 (FFA4) is a G protein-coupled receptor (GPCR) for long-chain fatty acids that functions as a regulator of physiological energy metabolism. In the present study, we aimed to investigate whether human eosinophils express GPR120 and, if present, whether it possesses a functional capacity on eosinophils. Eosinophils isolated from peripheral venous blood expressed GPR120 at both the mRNA and protein levels. Stimulation with a synthetic GPR120 agonist, GW9508, induced rapid down-regulation of cell surface expression of GPR120, suggesting ligand-dependent receptor internalization. Although GPR120 activation did not induce eosinophil chemotactic response and degranulation, we found that GW9508 inhibited eosinophil spontaneous apoptosis and Fas receptor expression. The anti-apoptotic effect was attenuated by phosphoinositide 3-kinase (PI3K) inhibitors and was associated with inhibition of caspase-3 activity. Eosinophil response investigated using ELISpot assay indicated that stimulation with a GPR120 agonist induced IL-4 secretion. These findings demonstrate the novel functional properties of fatty acid sensor GPR120 on human eosinophils and indicate the previously unrecognized link between nutrient metabolism and the immune system.
Highlights
The expression of GPR120 had been determined on monocytes/macrophages [10], its expression on human blood eosinophils is yet to be determined
We first investigated the surface receptor expression level using flow cytometry followed by stimulation with GW9508 since GPR120 has been shown to translocate from the plasma membrane to the cytosol rapidly after ligand stimulation [9,10]
To test whether phosphoinositide 3-kinase (PI3K) signaling was involved in the anti-apoptotic effect, we examined the effect of PI3K inhibitors on the GW9508-induced eosinophil survival
Summary
We aimed to investigate whether human eosinophils express GPR120 and, if present, whether it possesses a functional capacity on eosinophils
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