Emerging evidence suggests a pivotal role of macrophage migration inhibitory factor (MIF) in the systemic
inflammatory immune response. MIF is located in various cell types and rapidly released after different stimuli like
inflammation, surgical stress or ischemia and reperfusion. MIF is a known key player in the inflammatory response and
contributes to several biological functions including the control of cell cycle (through activation of ERK1/2), sensing of
pathogen stimuli (upregulation of TLR4 expression), recruitment of various immune cells (neutrophils, monocytes) and
prevention of p53-mediated apoptosis of macrophages. While MIF`s pro-inflammatory effects are crucial for an effective
host defense, elevated MIF levels were repeatedly shown to be associated with the development of organ dysfunction and
deleterious sequelae. Even more puzzling, increasing evidence indicates a protective role of this pleiotropic cytokine
during ischemia and reperfusion injury in the myocardium. This review focuses on new insights regarding the biological
significance of MIF release in the context of critical illness and ischemia/ reperfusion.
Keywords: Chemokine, critical illness, inflammation, macrophage migration inhibitory factor, multiple organ failure, sepsis,
systemic inflammatory response syndrome.
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