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Updated: Jun 22, 2026
Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages
Published on: August 12, 2019
Oxidoreductase Macrophage Migration Inhibitory Factor is simultaneously increased in leukocyte subsets of patients
Lutz E Lehmann1, Stefan U Weber, Dagmar Fuchs
1Klinik und Poliklinik für Anästhesie und operative Intensivmedizin, Universität Bonn, Bonn, Germany. Lutz.Lehmann@ukb.uni-bonn.de
Abstract:
The oxidoreductase Macrophage Migration Inhibitory Factor (MIF) is discussed as a promising target for immunomodulatory therapy in patients with severe sepsis. Moreover, MIF expresses tautomerase as well as thiol-protein oxidoreductase activities and has a potential role in cellular redox homeostasis, apoptosis inhibition, endotoxin responsiveness as well as regulation of nuclear transcription factors. To further elucidate a potential role of intracellular MIF in severe sepsis, we assessed alterations of intracellular MIF content in peripheral blood leukocytes of patients with severe sepsis in comparison to healthy controls and non-septic patients after major surgery. Intracellular MIF was significantly elevated simultaneously in lymphocytes, B-cells, macrophages and granulocytes of patients with severe sepsis when compared to healthy control individuals (p < 0.05) and increased when compared to non-septic patients after major surgery. In parallel, plasma MIF levels were elevated in severe sepsis (p < 0.05). There was no difference of intracellular MIF in lymphocytes, B-cells, macrophages or granulocytes between surviving and non-surviving patients with severe sepsis (p > 0.05). However, in survivors LPS ex vivo stimulation increased MIF secretion but not in non-survivors of sepsis (p < 0.05). This finding underlines the role of intracellular MIF in inflammatory diseases. It suggests monitoring of intracellular MIF in further clinical and non-clinical research valuable.
Insights
Intracellular Macrophage Migration Inhibitory Factor (MIF) is elevated in severe sepsis patients. MIF levels in survivors increase upon LPS stimulation, suggesting its role in inflammatory diseases and potential as a therapeutic target.
Area of Science:
- Immunology
- Molecular Biology
- Biochemistry
Background:
- Macrophage Migration Inhibitory Factor (MIF) is an oxidoreductase with roles in inflammation and immune response.
- MIF's involvement in cellular redox homeostasis, apoptosis, and transcription regulation is known.
- Severe sepsis presents a critical condition where immunomodulatory therapies are being explored.
Purpose of the Study:
- To investigate the alterations in intracellular Macrophage Migration Inhibitory Factor (MIF) content in peripheral blood leukocytes during severe sepsis.
- To compare intracellular MIF levels in severe sepsis patients with healthy controls and non-septic post-surgery patients.
- To explore the correlation between MIF levels, patient survival, and ex vivo lipopolysaccharide (LPS) stimulation.
Main Methods:
- Quantification of intracellular MIF in lymphocytes, B-cells, macrophages, and granulocytes from severe sepsis patients, healthy controls, and non-septic patients.
- Measurement of plasma MIF levels in severe sepsis patients.
- Ex vivo lipopolysaccharide (LPS) stimulation of leukocytes from sepsis survivors and non-survivors to assess MIF secretion.
Main Results:
- Intracellular MIF was significantly elevated in lymphocytes, B-cells, macrophages, and granulocytes of severe sepsis patients compared to healthy controls and non-septic patients.
- Plasma MIF levels were also elevated in patients with severe sepsis.
- While intracellular MIF levels did not differ between survivors and non-survivors, LPS stimulation ex vivo increased MIF secretion in survivors but not in non-survivors.
Conclusions:
- Intracellular MIF is significantly upregulated in peripheral blood leukocytes of patients with severe sepsis.
- The differential response to LPS stimulation in survivors versus non-survivors highlights the dynamic role of MIF in sepsis.
- Monitoring intracellular MIF may be valuable for future clinical and non-clinical research in inflammatory diseases.
