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Macrophage migration inhibitory factor is a critical mediator of severe acute pancreatitis
Yoshitaka Sakai1, Atsushi Masamune, Akihiko Satoh
1Division of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Background & Aims:
Macrophage migration inhibitory factor (MIF), originally described as an inhibitor of the random migration of macrophages, has been shown recently to be involved in the pathogenesis of several inflammatory diseases such as sepsis. The aim of this study was to clarify the role of MIF in acute pancreatitis (AP).
Methods:
Hemorrhagic necrotizing pancreatitis and edematous pancreatitis were induced by the injection of taurocholic acid (TCA pancreatitis) and cerulein (cerulein pancreatitis), respectively, on male Wistar rats. MIF levels in ascitic fluids, serum, and the organs were determined. The effects of anti-MIF antibody were examined on the prognosis of rats with TCA pancreatitis and of female CD-1 mice with choline-deficient, ethionine-supplemented, diet-induced model of severe AP. In addition, serum MIF levels in AP patients and in healthy controls were measured.
Results:
Serum and ascitic MIF levels in TCA pancreatitis were increased rapidly and decreased gradually thereafter. Ascitic MIF levels were also increased in cerulein pancreatitis, but to a lesser degree. MIF level was increased in the lung in TCA pancreatitis, but not in the pancreas and the liver. Prophylactic (1 hour before and immediately after induction) administration of anti-MIF antibody significantly improved the survival rate of rats with TCA pancreatitis. The survival rate of mice with severe AP was also improved significantly by the antibody treatment. Serum MIF levels were higher in severe AP patients than mild AP patients and healthy controls.
Conclusions:
These results suggest a role of MIF in the pathogenesis of severe AP.
Insights
Macrophage migration inhibitory factor (MIF) plays a role in severe acute pancreatitis (AP). Blocking MIF with antibodies improved survival in rat and mouse models of AP, suggesting MIF contributes to AP pathogenesis.
Area of Science:
- Immunology
- Gastroenterology
- Pathophysiology
Background:
- Macrophage migration inhibitory factor (MIF) is implicated in inflammatory diseases like sepsis.
- Its specific role in acute pancreatitis (AP) pathogenesis requires clarification.
Purpose of the Study:
- To investigate the role of MIF in the pathogenesis of acute pancreatitis (AP).
Main Methods:
- Induction of pancreatitis in Wistar rats and CD-1 mice using various models (TCA, cerulein, choline-deficient/ethionine-supplemented diet).
- Measurement of MIF levels in serum, ascitic fluid, and organs.
- Assessment of anti-MIF antibody effects on survival rates in pancreatitis models.
- Comparison of serum MIF levels in AP patients and healthy controls.
Main Results:
- Serum and ascitic MIF levels increased significantly in TCA-induced pancreatitis.
- Ascitic MIF levels were elevated in cerulein-induced pancreatitis.
- MIF levels increased in the lungs of rats with TCA pancreatitis.
- Anti-MIF antibody treatment improved survival in both rat and mouse AP models.
- Higher serum MIF levels were observed in severe AP patients compared to mild AP patients and controls.
Conclusions:
- MIF is involved in the pathogenesis of severe acute pancreatitis (AP).
- Targeting MIF may offer a therapeutic strategy for severe AP.
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01:27Acute Pancreatitis I: Introduction
Acute pancreatitis is characterized by rapid inflammation of the pancreas, often caused by factors like gallstone blockage or excessive alcohol consumption. Chronic pancreatitis, on the other hand, is a slow, progressive inflammation that may result from long-term alcohol abuse, obstructions in the pancreatic duct, or genetic factors.
The causes of acute pancreatitis include:
01:24Chronic Pancreatitis I: Introduction
Pancreatitis is the inflammation of the pancreas, which occurs when the immune system becomes active and causes swelling, pain, and disruptions in organ function. Pancreatitis can manifest as either an acute or chronic condition.
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01:25Chronic Pancreatitis I: Introduction
01:21Chronic Pancreatitis II: Pathophysiology