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The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
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TWEAK promotes peritoneal inflammation.

Ana Belen Sanz1, Luiz Stark Aroeira2, Teresa Bellon3

  • 1Laboratory of Nephrology, IIS-Fundacion Jimenez Diaz, Madrid, Spain; REDinREN, Madrid, Spain.

Plos One
|March 7, 2014
PubMed
Summary
This summary is machine-generated.

The TWEAK/Fn14 system may worsen inflammation and tissue damage during peritoneal dialysis peritonitis. Targeting this pathway could potentially reduce peritoneal injury in patients undergoing dialysis.

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Area of Science:

  • Nephrology
  • Immunology
  • Cell Biology

Background:

  • Peritoneal dialysis (PD) is susceptible to peritonitis, leading to mesothelial cell loss and sclerosing peritonitis.
  • Understanding molecular mechanisms of peritoneal injury is crucial for developing new therapies.
  • The role of the TWEAK/Fn14 cytokine system in PD-related peritoneal injury was previously unknown.

Purpose of the Study:

  • To investigate the expression and function of the TWEAK/Fn14 system in the context of peritoneal injury during PD.
  • To determine if TWEAK/Fn14 signaling contributes to inflammation and tissue damage in PD patients and a mouse model.

Main Methods:

  • Measured soluble TWEAK (sTWEAK) levels and Fn14 expression in human PD effluent and biopsies.
  • Analyzed TWEAK/Fn14 expression in mesothelial cells and macrophages.
  • Administered TWEAK intraperitoneally in mice to assess its effects on peritoneal inflammation.

Main Results:

  • Elevated sTWEAK levels and increased Fn14 expression were observed in PD patients with peritonitis.
  • sTWEAK levels correlated with peritoneal macrophage counts.
  • Fn14 expression in peritoneal biopsies correlated with mesothelial injury, fibrosis, and inflammation.
  • TWEAK administration in mice induced peritoneal inflammation, macrophage recruitment, and expression of inflammatory mediators.

Conclusions:

  • The TWEAK/Fn14 system is upregulated during PD peritonitis and is associated with peritoneal inflammation and tissue injury.
  • This system, involving mesothelial cells and macrophages, appears to play a detrimental role in PD-related peritoneal complications.
  • Targeting the TWEAK/Fn14 pathway may offer a therapeutic strategy to mitigate peritoneal injury in PD patients.