Deficiency of the macrophage migration inhibitory factor gene has no significant effect on endotoxaemia

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Abstract
By targeted disruption of the MIF gene, we have established a mouse strain deficient in macrophage (Mφ) migration inhibitory factor (MIF). Despite previous reports indicating an essential role of MIF in endotoxaemia, an injection of lipopolysaccharide (LPS) into the MIF-deficient mice (maintained under specific pathogen-free conditions) caused shock. No significant difference was detected between the MIF-deficient mutant and normal mice in susceptibility to LPS for endotoxaemia or tumour necrosis factor-α (TNF-α) formation upon LPS injection. Peritoneal Mφ from the two strains produced TNF-α in response to LPS with similar dose responses. Dexamethasone suppressed the LPS-induced TNF-α response of Mφ, but no difference was detected between the Mφ from the two strains. These results suggest that endogenous MIF has no significant effect on the LPS-induced TNF-α production and no effect on suppression of the response by glucocorticoids. Thus, MIF is not crucial for LPS-induced immune responses leading to shock.