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Updated: Dec 26, 2025
Alveolar Macrophage Phagocytosis and Bacteria Clearance in Mice
Published on: March 2, 2019
The GPR120 Agonist TUG-891 Inhibits the Motility and Phagocytosis of Mouse Alveolar Macrophages
Xing-Li Su1, Ying-Guang Liu1, Man Shi1
1Institute of Basic Medical Sciences, Xi'an Medical University, Xi'an 710021, China.
Abstract:
Movement and phagocytosis characterize the fundamental actions of macrophages. Although it is known that the free fatty acid receptor GPR120 is expressed in macrophages and regulates cytokine expression to exert anti-inflammatory activities, the effects of GPR120 activation on the motility and phagocytosis of macrophages are not clear. In this study, mouse alveolar macrophages (AM) were stimulated with the GPR120 agonist TUG-891, and the changes in cell motility, intracellular Ca2+ concentration ([Ca2+]i), and the ability of phagocytosis were measured. Mouse AM in controls exhibited active movement in vitro, and TUG-891 significantly restrained AM movement. Meanwhile, TUG-891 stimulated a quick increase in [Ca2+]i in AM, which was blocked separately by the Gq protein inhibitor YM-254890, the phospholipase C (PLC) inhibitor U73122, or depletion of endoplasmic reticulum (ER) Ca2+ store by thapsigargin. The inhibition of AM movement by TUG-891 was eliminated by YM-254890, U73122, thapsigargin, and chelation of cytosolic Ca2+ by BAPTA. Moreover, TUG-891 inhibited AM phagocytosis of fluorescent microspheres, which was also blocked by YM-254890, U73122, thapsigargin, and BAPTA. In conclusion, GPR120 activation in mouse AM increases [Ca2+]i but inhibits the motility and phagocytosis via Gq protein/PLC-mediated Ca2+ release from ER Ca2+ store.
Insights
Activation of GPR120 in mouse macrophages increases intracellular calcium but inhibits cell movement and phagocytosis. This occurs through a Gq protein/PLC-mediated pathway involving endoplasmic reticulum calcium release.
Area of Science:
- Immunology
- Cell Biology
- Pharmacology
Background:
- Macrophages are key immune cells involved in movement and phagocytosis.
- The free fatty acid receptor GPR120 is present in macrophages and influences cytokine expression.
- The impact of GPR120 activation on macrophage motility and phagocytosis remains unclear.
Purpose of the Study:
- To investigate the effects of GPR120 activation on mouse alveolar macrophage (AM) motility and phagocytosis.
- To elucidate the signaling pathways involved in GPR120-mediated effects on AM function.
Main Methods:
- Mouse AM were stimulated with the GPR120 agonist TUG-891.
- Measurements included cell motility, intracellular calcium concentration ([Ca2+]i), and phagocytic activity.
- Pharmacological inhibitors (YM-254890, U73122, thapsigargin, BAPTA) were used to probe signaling pathways.
Main Results:
- TUG-891 significantly inhibited AM movement and phagocytosis of microspheres.
- TUG-891 induced a rapid increase in [Ca2+]i, mediated by Gq protein/PLC and endoplasmic reticulum (ER) Ca2+ release.
- Inhibitors of the Gq/PLC pathway and Ca2+ chelation abolished the inhibitory effects of TUG-891 on motility and phagocytosis.
Conclusions:
- GPR120 activation in mouse AM elevates intracellular calcium levels.
- GPR120 activation inhibits macrophage motility and phagocytosis via a Gq protein/PLC-dependent pathway.
- This pathway involves calcium release from the ER, impacting fundamental macrophage functions.
