Does macrophage migration inhibitory factor function as a switch in septic circulation crisis?

Abstract

Circulation dysfunction-associated mortality is defined as its reduced responsiveness to circulation active agents in the pathological context of sepsis/septic shock. Macrophage migration inhibitory factor (MIF), a versatile pro-inflammatory cytokine, has been identified independently from other mediators and found to play certain roles in the “bio-vicious-gate” of circulation collapse. Cumulating evidence shows that MIF exerts its function through interaction with a body of signal molecules that are involved in functional regulation of several end-point molecules such as, carbon monoxide, insulin, complement C5a, nitric oxide, inducible nitric oxide synthase, and glucocorticoids, and these downstream mediators are linked to vascular tone differentially. Thus, MIF stays as a molecular switch at the signaling upstream to charge the downstream action of signals in sepsis-associated circulation crisis.

Keywords: Sepsis; Macrophage migration inhibitory factor; Circulation dysfunction; Cytokine

Internet Journal of Medical Update Vol. 3 (2) 2008: pp. 40-45