Macrophage Migration Inhibitory Factor Contributes to Host Defense against Acute<i>Trypanosoma cruzi</i>Infection

Reyes, José L.; Terrazas, Luis I.; Espinoza, Bertha; Cruz-Robles, David; Soto, Virgilia; Rivera-Montoya, Irma; Gómez-García, Lorena; Snider, Heidi; Satoskar, Abhay R.; Rodrı́guez-Sosa, Miriam

doi:10.1128/iai.01648-05

Cited by 81 publications

(62 citation statements)

References 70 publications

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“…22,23,25,26 MIF expression requires interaction with other proinflammatory cytokines such as IFN-␥. 25 Subsequently, MIF acts by binding to its receptor complex (CD74 -CD44), 38,47 thereby activating a signal transduction pathway, 48 gene transcription, and expression of effector molecules such as cytokines 24 and adhesion molecules. 25 The proinflammatory activity of MIF was recently demonstrated to control T. gondii infection because, compared with wild-type mice, MIF Ϫ/Ϫ mice exhibited greater liver damage, more brain cysts, and less proinflammatory cytokine production, and succumbed to infection faster, which indicates a critical role of MIF in mediating host resistance against T. gondii.…”

Section: Discussionmentioning

confidence: 99%

“…30 The volume of villus explants was determined as previously described. 24 In brief, 800 L medium was placed in a pipette and the villus explant was added, which became totally submerged in the medium. The amount of increased volume was assumed as the villus volume.…”

Section: Placenta Samples and Human Chorionic Villus Explant Culturesmentioning

confidence: 99%

“…MIF has a multifaceted role in immune responses such as phagocytosis, inflammation, and inhibition of neutrophil apoptosis. 19,20 In addition, it is an important factor in determining the outcome of infections caused by protozoan parasites such as Plasmodium chabaudi, 21 P. falciparum, 22 Leishmania major, 23 Trypanosoma cruzi, 24 and T. gondii, 25,26,27 and in helminth (Taenia crassiceps) 28 and bacterial (Salmonella typhimurium) 29 infections.…”

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confidence: 99%

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Effect of Macrophage Migration Inhibitory Factor (MIF) in Human Placental Explants Infected with Toxoplasma gondii Depends on Gestational Age

Gomes¹,

Silva²,

Silva³

et al. 2011

The American Journal of Pathology

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Because macrophage migration inhibitory factor (MIF) is a key cytokine in pregnancy and has a role in inflammatory response and pathogen defense, the objective of the present study was to investigate the effects of MIF in first-and third-trimester human placental explants infected with Toxoplasma gondii. Explants were treated with recombinant MIF, IL-12, interferon-␥, transforming growth factor-␤1, or IL-10, followed by infection with T. gondii RH strain tachyzoites. Supernatants of cultured explants were assessed for MIF production. Explants were processed for morphologic analysis, immunohistochemistry, and real-time PCR analysis. Comparison of infected and stimulated explants versus noninfected control explants demonstrated a significant increase in MIF release in first-trimester but not third-trimester explants. Tissue parasitism was higher in third-than in first-trimester explants. Moreover, T. gondii DNA content was lower in first-trimester explants treated with MIF compared with untreated explants. However, in third-trimester explants, MIF stimulus decreased T. gondii DNA content only at the highest concentration of the cytokine. In addition, high expression of MIF receptor was observed in first-trimester placental explants, whereas MIF receptor expression was low in third-trimester explants. In conclusion, MIF was up-regulated and demonstrated to be important for control of T. gondii infection in first-trimester explants, whereas lack of MIF up-regulation in third-trimester placentas may be involved in higher susceptibility to infection at this gestational age.

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Section: Discussionmentioning

confidence: 99%

Section: Placenta Samples and Human Chorionic Villus Explant Culturesmentioning

confidence: 99%

mentioning

confidence: 99%

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Effect of Macrophage Migration Inhibitory Factor (MIF) in Human Placental Explants Infected with Toxoplasma gondii Depends on Gestational Age

Gomes¹,

Silva²,

Silva³

et al. 2011

The American Journal of Pathology

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“…It is believed that the global proinflammatory effect of MIF is mainly due to its ability to override activation-induced apoptosis in monocytes/macrophages, which in turn further activates and sustains inflammatory responses (20,29). Although the MIF-dependent induction of inflammatory cytokines has been shown to be protective against Salmonella typhimurium (30), Leishmania major (31), and Trypanosoma cruzi (32), high MIF levels are deleterious in endotoxic and exotoxic shock (33,34) and in polymicrobial sepsis (14). The role of MIF in infection caused by neurotropic viruses has not previously been studied; however, an exacerbated inflammatory response can be extremely detrimental, since inflammatory cytokines have been shown to increase the permeability of the BBB (9,(23)(24)(25)(35)(36)(37).…”

Section: Discussionmentioning

confidence: 99%

Abrogation of macrophage migration inhibitory factor decreases West Nile virus lethality by limiting viral neuroinvasion

Arjona¹,

Foellmer²,

Town³

et al. 2007

J. Clin. Invest.

142

149

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The flavivirus West Nile virus (WNV) is an emerging pathogen that causes life-threatening encephalitis in susceptible individuals. We investigated the role of the proinflammatory cytokine macrophage migration inhibitory factor (MIF), which is an upstream mediator of innate immunity, in WNV immunopathogenesis. We found that patients suffering from acute WNV infection presented with increased MIF levels in plasma and in cerebrospinal fluid. MIF expression also was induced in WNV-infected mice. Remarkably, abrogation of MIF action by 3 distinct approaches (antibody blockade, small molecule pharmacologic inhibition, and genetic deletion) rendered mice more resistant to WNV lethality. Mif -/-mice showed a reduced viral load and inflammatory response in the brain when compared with wild-type mice. Our results also indicate that MIF favors viral neuroinvasion by compromising the integrity of the blood-brain barrier. In conclusion, the data obtained from this study provide direct evidence for the involvement of MIF in viral pathogenesis and suggest that pharmacotherapeutic approaches targeting MIF may hold promise for the treatment of WNV encephalitis.

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“…Durante a infecção por T.cruzi, o IFN-γ é capaz de inibir in vitro o seu desenvolvimento (PLATA et al, 1984;REYES et al, 2006) e in vivo é capaz de diminuir a parasitemia e prolongar a sobrevida de animais infectados (PLATA et al, 1987;TORRICO et al, 1991;MICHAILOWSKY et al, 2001).…”

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Orquiectomia e administração de dehidroepiandrosterona (DHEA) em ratos Wistar infectados com 'Trypanosoma cruzi'

Filipin¹

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Macrophage Migration Inhibitory Factor Contributes to Host Defense against AcuteTrypanosoma cruziInfection

Abstract: Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that is involved in the host

Cited by 81 publications

References 70 publications

Effect of Macrophage Migration Inhibitory Factor (MIF) in Human Placental Explants Infected with Toxoplasma gondii Depends on Gestational Age

Effect of Macrophage Migration Inhibitory Factor (MIF) in Human Placental Explants Infected with Toxoplasma gondii Depends on Gestational Age

Abrogation of macrophage migration inhibitory factor decreases West Nile virus lethality by limiting viral neuroinvasion

Orquiectomia e administração de dehidroepiandrosterona (DHEA) em ratos Wistar infectados com 'Trypanosoma cruzi'

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