scholarly journals Macrophage Migration Inhibitory Factor Reduces the Growth of Virulent Mycobacterium tuberculosis in Human Macrophages

2005 ◽  
Vol 73 (6) ◽  
pp. 3783-3786 ◽  
Author(s):  
Mauro Oddo ◽  
Thierry Calandra ◽  
Richard Bucala ◽  
Pascal R. A. Meylan
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Migration Inhibitory Factor ◽  
Innate Immune System ◽  
Host Response ◽  
Macrophage Migration Inhibitory Factor ◽  
Bacterial Infections ◽  
Innate Immune ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Human Macrophages

ABSTRACT Macrophage migration inhibitory factor (MIF) is a key mediator of the innate immune system and plays a crucial role in the host response to bacterial infections. Its role in immunity to intracellular pathogens has not been well studied. Here, we show that MIF released by infected human macrophages inhibits the growth of virulent Mycobacterium tuberculosis.

scholarly journals Improved Resistance to Bacterial Superinfection in Mice by Treatment with Macrophage Migration Inhibitory Factor

2005 ◽  
Vol 73 (10) ◽  
pp. 6488-6492 ◽  
Author(s):  
N. Pollak ◽  
T. Sterns ◽  
B. Echtenacher ◽  
D. N. Männel
Keyword(s):  
Immune Suppression ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Bacterial Infections ◽  
Cecal Ligation ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Innate Immune Responses ◽  
Produce Tumor Necrosis Factor ◽  
Bacterial Superinfection

ABSTRACT Nosocomial infections in immune-suppressed patients are a widespread problem in intensive care medicine. Such patients are highly susceptible to infections because their immune defenses are impaired and, therefore, unable to adequately combat invading microorganisms. To investigate the problem of sepsis-induced immune suppression, we used a model in which mice developed sublethal peritonitis induced by cecal ligation and puncture (CLP). Two days after CLP mice were in an immune-suppressed state, as measured by impaired capacity to produce tumor necrosis factor (TNF) and enhanced susceptibility to bacterial infections. Since macrophage migration inhibitory factor (MIF) is a critical mediator of septic shock by modulation of innate immune responses, the role of MIF in sepsis-induced immune suppression was analyzed. Neutralization of endogenous MIF further enhanced susceptibility to bacterial superinfection after CLP. Conversely, treatment with recombinant human MIF before the bacterial superinfection protected the animals. MIF treatment reconstituted the impaired capacity to produce proinflammatory cytokines, such as TNF and interleukin-6. This study indicates that MIF might be able to ameliorate the sepsis-induced immune suppression by reenabling the organism to react adequately to a secondary bacterial challenge.

Critical role of macrophage migration inhibitory factor in sepsis via interfere with MCP-1/CCL2 signaling pathway

2015 ◽  
Vol 3 (3) ◽  
pp. 215-228
Author(s):  
Jason J Goodman ◽  
Alison A Putensen
Keyword(s):  
Adhesion Molecule ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Bacterial Infections ◽  
Critical Role ◽  
Cecal Ligation ◽  
Inhibitory Factor ◽  
Intercellular Adhesion Molecule ◽  
Macrophage Migration

Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine produced by the multiple cell types, modulates the expression of several inflammatory molecules. Since MIF is a critical mediator of septic shock by modulation of innate immune responses and many studies demonstrated the role of MIF in sepsis pathogenesis and signaling pathways; however, the mechanisms underlying these changes remain unclear. MIF also promotes the migration and recruitment of immune cells inducing the expression of chemokines (monocyte chemoattractant protein (MCP)-1, adhesion molecules as intercellular adhesion molecule (I-CAM)-1 and vascular cell adhesion molecule (V-CAM)-1. Male MIF+/+ and MIF−/− mice were subjected to cecal ligation and puncture (CLP) to induce sepsis. Mif(-/-) mice had enhanced susceptibility to bacterial infections and impaired tumor necrosis factor (TNF) compared with MIF+/+. Further, Mif(-/-) mice showed upregulation of proinflammatory cytokine and eleveated the levels of MCP-1. Interesting treatment with recombinant human MIF (rhMIF) before CLP protected the animals from sepsis. Together, these data suggest that potential of targeting or exploiting MIF for therapeutic strategies in the management of sepsis.

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