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Background  Patients infected with  Vibrio vulnificus (V. vulnificus)  show severe inflammatory responses characterised by the upregulation of proinflammatory cytokines. Macrophage migration inhibitory factor (MIF), an upstream proinflammatory regulator, increases the inflammation caused by sepsis. Whether MIF regulates responses to  V. vulnificus  infection and the actual mechanism by which  V. vulnificus  initiates these MIF-modulated proinflammatory cytokines remain unclear.    Results  MIF increased inflammation during  V. vulnificus  infection  in vivo . In  V. vulnificus -infected mice, MIF was produced earlier than tumour necrosis factor (TNF)-α and interleukin (IL)-6 and was expressed in a time-dependent manner. ISO-1 ((S, R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester), a small-molecule inhibitor of MIF, significantly decreased IL-6, IL-8, and TNF-α production in a time- and dose-dependent manner in human peripheral blood cells infected with  V. vulnificus . The induction of IL-6, IL-8, and TNF-α production by  V. vulnificus  infection was mediated via the NF-κB- and p38 MAPK-regulated pathways but not via the Akt pathway. ISO-1-treated human peripheral blood cells showed lower  V. vulnificus -induced NF-κB activation, IL-6 mRNA expression, and IκB phosphorylation, but they did not show lower p38 MAPK activation.    Conclusions  We conclude that MIF regulates  V. vulnificus -induced IL-6 production via NF-κB activation and that p38 MAPK activation in  V. vulnificus  infection is not MIF dependent.

bmc immunology

Macrophage migration inhibitory factor regulates interleukin-6 production by facilitating nuclear factor-kappa B activation during Vibrio vulnificus infection