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Updated: Oct 2, 2026
Long Term Intravital Multiphoton Microscopy Imaging of Immune Cells in Healthy and Diseased Liver Using CXCR6.Gfp Reporter Mice
Published on: March 24, 2015
Graft-derived macrophage migration inhibitory factor correlates with hepatocellular injury in patients undergoing
Joanna Baron-Stefaniak1, Judith Schiefer1, Edmund J Miller2
1Department of Anesthesia, General Intensive Care and Pain Management, Medical University of Vienna, Vienna, Austria.
Abstract:
Experimental studies suggest that macrophage migration inhibitory factor (MIF) mediates ischemia/reperfusion injury during liver transplantation. This study assessed whether human liver grafts release MIF during preservation, and whether the release of MIF is proportional to the extent of hepatocellular injury. Additionally, the association between MIF and early allograft dysfunction (EAD) after liver transplantation was evaluated. Concentrations of MIF, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and creatine kinase (CK) were measured in effluents of 38 liver grafts, and in serum of recipients. Concentrations of MIF in the effluent were greater than those in the recipients' serum before and after reperfusion (58 [interquartile range, IQR:23-79] μg/mL vs 0.06 [IQR:0.03-0.07] μg/mL and 1.3 [IQR:0.7-1.8] μg/mL, respectively; both P<.001). Effluent MIF concentrations correlated with effluent concentrations of the cell injury markers ALT (R=.51, P<.01), AST (R=.51, P<.01), CK (R=.45, P=.01), and LDH (R=.56, P<.01). Patients who developed EAD had greater MIF concentrations in effluent and serum 10 minutes after reperfusion than patients without EAD (Effluent: 80 [IQR:63-118] μg/mL vs 36 [IQR:20-70] μg/mL, P=.02; Serum: 1.7 [IQR:1.2-2.5] μg/mL vs 1.1 [IQR:0.6-1.7] μg/mL, P<.001).
Conclusion:
Human liver grafts release MIF in proportion to hepatocellular injury. Greater MIF concentrations in effluent and recipient's serum are associated with EAD after liver transplantation.
Insights
Human liver grafts release macrophage migration inhibitory factor (MIF) proportionally to liver injury. Higher MIF levels in graft effluent and recipient serum correlate with early allograft dysfunction after transplantation.
Area of Science:
- Transplantation immunology
- Organ preservation research
- Biomarker discovery
Background:
- Macrophage migration inhibitory factor (MIF) is implicated in ischemia/reperfusion injury.
- Understanding MIF's role in liver transplantation is crucial for improving outcomes.
Purpose of the Study:
- To determine if human liver grafts release MIF during preservation.
- To assess if MIF release correlates with hepatocellular injury.
- To evaluate the association between MIF and early allograft dysfunction (EAD).
Main Methods:
- Measurement of MIF, AST, ALT, LDH, and CK in liver graft effluents and recipient serum from 38 patients.
- Correlation analysis between MIF concentrations and liver injury markers.
- Comparison of MIF levels in patients with and without EAD.
Main Results:
- Human liver grafts release significantly higher concentrations of MIF in effluent compared to recipient serum.
- Effluent MIF levels positively correlated with hepatocellular injury markers (ALT, AST, CK, LDH).
- Elevated MIF concentrations in effluent and serum were associated with EAD post-transplantation.
Conclusions:
- Human liver grafts release MIF in proportion to the extent of hepatocellular injury.
- Increased MIF levels in graft effluent and recipient serum are linked to EAD following liver transplantation.
