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Lipopolysaccharide inhibits GPR120 expression in macrophages via Toll-like receptor 4 and p38 MAPK activation

Yan-Yan Zhao1, Hui Fu1, Xiang-Yan Liang1

  • 1Institute of Basic Medical Sciences, Xi'an Medical University, Xi'an, 710021, China.

Cell Biology International
|July 20, 2019
PubMed

Insights

Lipopolysaccharide (LPS) inhibits the expression and activation of free fatty acid receptor G protein-coupled receptor 120 (GPR120) in macrophages. This inhibition enhances the pro-inflammatory response, impacting macrophage function during inflammation.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Macrophages play a critical role in inflammatory responses.
  • Free fatty acid receptor G protein-coupled receptor 120 (GPR120) is expressed in macrophages and can inhibit pro-inflammatory cytokine production.
  • The effect of lipopolysaccharide (LPS) on GPR120 expression and signaling in macrophages during inflammation is not well understood.

Purpose of the Study:

  • To investigate the impact of LPS on macrophage GPR120 expression and activation.
  • To elucidate the signaling pathways involved in LPS-mediated regulation of GPR120.
  • To understand how LPS affects GPR120-mediated functions, such as phagocytosis.

Main Methods:

  • Treatment of mouse macrophage cell line (Ana-1) and primary mouse alveolar macrophages with LPS.
  • Assessment of GPR120 expression levels.
  • Inhibition of Toll-like receptor 4 (TLR4) and specific kinases (p38 MAPK, ERK1/2, JNK).
  • Administration of GPR120 agonists (TUG891, GW9508).
  • Evaluation of macrophage phagocytic activity.

Main Results:

  • LPS significantly inhibited GPR120 expression in macrophages, both in vitro and in vivo.
  • The inhibitory effect of LPS on GPR120 expression was mediated through Toll-like receptor 4 (TLR4) and the p38 MAPK pathway.
  • LPS did not affect GPR120 activation by agonists but counteracted the inhibitory effect of a GPR120 agonist on macrophage phagocytosis.
  • LPS pretreatment inhibited GPR120 expression and activation in macrophages.

Conclusions:

  • LPS treatment downregulates GPR120 expression and activation in macrophages.
  • This downregulation is dependent on TLR4 and p38 MAPK signaling.
  • The inhibition of GPR120 by LPS may contribute to an enhanced pro-inflammatory response in macrophages.
  • Understanding this mechanism provides insights into macrophage behavior during inflammatory conditions.
Keywords:
GPR120lipopolysaccharidemacrophagetoll-like receptor 4

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