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Caerulin-induced pro-inflammatory response in macrophages requires TRAF3-p38 signaling activation

Rongrong Jia1, Jiali Ma1, Shihao Xiang1

  • 1Department of Gastroenterology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Biochemical and Biophysical Research Communications
|October 9, 2017
PubMed

Insights

Tumor necrosis factor receptor-associated factor 3 (TRAF3) drives inflammation in acute pancreatitis. Inhibiting TRAF3 in macrophages reduces inflammatory responses and pancreatic cell damage, suggesting TRAF3 as a therapeutic target.

Area of Science:

  • Immunology
  • Cell Biology
  • Gastroenterology

Background:

  • Acute pancreatitis is a significant health concern characterized by inflammation and pancreatic cell injury.
  • Caerulin is a known inducer of severe inflammation in pancreatic tissues.
  • Tumor necrosis factor receptor-associated factor 3 (TRAF3) is a key regulator of immune responses.

Purpose of the Study:

  • To investigate the role of TRAF3 in caerulin-induced pro-inflammatory responses in acute pancreatitis.
  • To determine if TRAF3 is a potential therapeutic target for acute pancreatitis treatment.

Main Methods:

  • Primary-cultured mouse bone marrow-derived macrophages (BMDMs) were stimulated with caerulin.
  • TRAF3 protein stabilization and its complex formation with MKK3 were analyzed.
  • TRAF3 was stably knocked down using lentiviral shRNA to assess its impact on downstream signaling and cytokine production.

Main Results:

  • Caerulin induced TRAF3 stabilization, leading to MKK3-p38 pathway activation.
  • TRAF3 knockdown significantly reduced caerulin-induced MKK3-p38 activation and the production of pro-inflammatory cytokines (IL-1β, TNF-α, IL-17).
  • TRAF3 inhibition also decreased cytotoxicity to pancreatic cells (Panc02 and primary mouse pancreatic cells).

Conclusions:

  • TRAF3 is essential for mediating caerulin-induced p38 activation and pro-inflammatory responses in macrophages.
  • TRAF3 plays a critical role in the pathogenesis of acute pancreatitis.
  • Targeting TRAF3 expression in macrophages presents a novel therapeutic strategy for acute pancreatitis.
Keywords:
Acute pancreatitisCaerulinMacrophagesPro-inflammatory responsesTRAF3p38

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