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pubmed-article:10809963pubmed:abstractTextBy targeted disruption of the MIF gene, we have established a mouse strain deficient in macrophage (Mphi) 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-alpha (TNF-alpha) formation upon LPS injection. Peritoneal Mphi from the two strains produced TNF-alpha in response to LPS with similar dose responses. Dexamethasone suppressed the LPS-induced TNF-alpha response of Mphi, but no difference was detected between the Mphi from the two strains. These results suggest that endogenous MIF has no significant effect on the LPS-induced TNF-alpha production and no effect on suppression of the response by glucocorticoids. Thus, MIF is not crucial for LPS-induced immune responses leading to shock.lld:pubmed
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pubmed-article:10809963pubmed:authorpubmed-author:NakayamaTTlld:pubmed
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pubmed-article:10809963pubmed:dateRevised2009-11-18lld:pubmed
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pubmed-article:10809963pubmed:articleTitleDeficiency of the macrophage migration inhibitory factor gene has no significant effect on endotoxaemia.lld:pubmed
pubmed-article:10809963pubmed:affiliationPharmaceutical Research Laboratory, Kirin Brewery Co. Ltd, Gunma, Japan.lld:pubmed
pubmed-article:10809963pubmed:publicationTypeJournal Articlelld:pubmed
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