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Deficiency of the macrophage migration inhibitory factor gene has no significant effect on endotoxaemia
Author(s) -
Honma N.,
Koseki H.,
Akasaka T.,
Nakayama T.,
Taniguchi M.,
Serizawa I.,
Akahori H.,
Osawa M.,
Mikayama T.
Publication year - 2000
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2000.00011.x
Subject(s) - macrophage migration inhibitory factor , lipopolysaccharide , tumor necrosis factor alpha , immune system , macrophage , biology , medicine , endocrinology , cytokine , dexamethasone , immunology , in vitro , biochemistry
Summary 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.