title: Oxidoreductase Macrophage Migration Inhibitory Factor is simultaneously increased in leukocyte subsets of patients with severe sepsis.
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.
authors.affiliation: Klinik und Poliklinik für Anästhesie und operative Intensivmedizin, Universität Bonn, Bonn, Germany. Lutz.Lehmann@ukb.uni-bonn.de
authors.forename: Lutz E
authors.initials: LE
authors.lastname: Lehmann
authors.forename: Stefan U
authors.initials: SU
authors.lastname: Weber
authors.forename: Dagmar
authors.initials: D
authors.lastname: Fuchs
authors.forename: Malte
authors.initials: M
authors.lastname: Book
authors.forename: Sven
authors.initials: S
authors.lastname: Klaschik
authors.forename: Jens-Christian
authors.initials: JC
authors.lastname: Schewe
authors.forename: Andreas
authors.initials: A
authors.lastname: Hoeft
authors.forename: Frank
authors.initials: F
authors.lastname: Stüber
mesh_terms: D015703:Antigens, CD / Q000097:blood; D018941:Antigens, CD19 / Q000097:blood; D017252:CD3 Complex / Q000097:blood; D015704:CD4 Antigens / Q000097:blood; D016827:CD8 Antigens / Q000097:blood; D015815:Cell Adhesion Molecules / Q000097:blood; D005260:Female; D058851:GPI-Linked Proteins; D006801:Humans; D007962:Leukocytes / Q000201:enzymology*; D018950:Lipopolysaccharide Receptors / Q000097:blood; D016131:Lymphocyte Subsets / Q000201:enzymology; D008263:Macrophage Migration-Inhibitory Factors / Q000097:blood*; D008297:Male; D010088:Oxidoreductases / Q000097:blood*; D018805:Sepsis / Q000097:blood* / Q000201:enzymology / Q000401:mortality
chemical_list: D015703:Antigens, CD; D018941:Antigens, CD19; D017252:CD3 Complex; D015704:CD4 Antigens; D016827:CD8 Antigens; C504120:CEACAM8 protein, human; D015815:Cell Adhesion Molecules; D058851:GPI-Linked Proteins; D018950:Lipopolysaccharide Receptors; D008263:Macrophage Migration-Inhibitory Factors; D010088:Oxidoreductases