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Updated: Aug 5, 2026

Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection
07:38

Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection

Published on: May 10, 2024

FCER1G-Notch1 mediated M1 macrophages polarization and pancreatic acinar cells death in acute pancreatitis

Hongjuan Ouyang1, Juan Zhou1, Jun Li2

  • 1Department of Gastroenterology and Nutrition, The Affiliated Children's Hospital of Xiangya School of Medicine, Central South University (Hunan Children's Hospital), Hunan Provincial Key Laboratory of Pediatric Orthopedics, Changsha, Hunan, China.

Experimental Cell Research
|July 30, 2026
PubMed

Insights

FCER1G and Notch1 are key in acute pancreatitis (AP) development by driving M1 macrophage polarization. Inhibiting FCER1G shows promise for treating AP through the Notch1 pathway.

Area of Science:

  • Gastroenterology
  • Immunology
  • Cell Biology

Background:

  • Acute pancreatitis (AP) involves pancreatic enzyme overactivation and inflammation.
  • M1 macrophage polarization is critical in AP pathogenesis.

Purpose of the Study:

  • To investigate the roles of FCER1G and Notch1 in M1 macrophage polarization during AP.
  • To explore FCER1G and Notch1 as potential therapeutic targets for AP.

Main Methods:

  • Studied FCER1G expression and Notch1 activity in LPS-induced M1 macrophages.
  • Utilized gene knockdown techniques for FCER1G and Notch1.
  • Assessed M1 macrophage polarization and pancreatic acinar cell (PAC) damage.
  • Investigated FCER1G's interaction with Notch1.
  • Evaluated FCER1G inhibition in a mouse model of AP.

Main Results:

  • FCER1G and Notch1 were upregulated in LPS-induced M1 macrophages.
  • Knockdown of FCER1G or Notch1 reduced inflammation and PAC damage.
  • FCER1G regulates Notch1 interaction to promote M1 polarization and PAC damage.
  • FCER1G inhibition alleviated AP injury via the Notch1 pathway in mice.

Conclusions:

  • FCER1G and Notch1 play vital roles in M1 macrophage polarization and AP progression.
  • FCER1G influences AP pathogenesis by regulating Notch1 interactions.
  • FCER1G presents a novel therapeutic target for acute pancreatitis.
Keywords:
FCER1GMacrophagesNotch1PancreatitisPolarization

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