Toxoplasma gondii: Impaired maturation and pro-inflammatory response of dendritic cells in MIF-deficient mice favors susceptibility to infection

Terrazas, César; Juárez, Imelda; Terrazas, Luis I.; Saavedra, Rafael; Calleja, Elsa A.; Rodrı́guez-Sosa, Miriam

doi:10.1016/j.exppara.2010.03.009

Cited by 38 publications

(41 citation statements)

References 45 publications

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“…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. 26,27 To our knowledge, our group was the first to associate MIF with congenital toxoplasmosis, although the entire mechanism responsible for mediating this protection still needs to be clarified. 25 It is possible that these mechanisms of control are independent of NO because NO was not detected in the experiments even after MIF stimulation.…”

Section: Discussionmentioning

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.…”

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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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%

mentioning

confidence: 99%

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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“…All the above-described inherent properties permitted the recognition of MIF as a critical molecule in proinflammatory innate immune responses and the restriction of certain parasite infections [12–14]. Additionally, MIF involvement has been demonstrated in immunological and inflammatory diseases [15, 16] such as septic shock [17], cancer [18], and chronic diseases including bowel disease [19], rheumatoid arthritis [20–22], colitis [23], obesity [24–26], and diabetes [25, 27, 28].…”

Section: Introductionmentioning

confidence: 99%

The Role of MIF in Type 1 and Type 2 Diabetes Mellitus

Sánchez-Zamora

Rodrı́guez-Sosa

2014

Journal of Diabetes Research

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Autoimmunity and chronic low-grade inflammation are hallmarks of diabetes mellitus type one (T1DM) and type two (T2DM), respectively. Both processes are orchestrated by inflammatory cytokines, including the macrophage migration inhibitory factor (MIF). To date, MIF has been implicated in both types of diabetes; therefore, understanding the role of MIF could affect our understanding of the autoimmune or inflammatory responses that influence diabetic pathology. This review highlights our current knowledge about the involvement of MIF in both types of diabetes in the clinical environment and in experimental disease models.

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“…These findings were expected considering that MIF is an enhancer of IL-12 and TNF production by macrophages. A recent study using a model of oral T. gondii infection in the BALB/c background also demonstrated an increased lethality and tissue parasitism with reduced IL-12 production and DC activation on Mif − / − mice compared to wild-type mice [41]. DCs obtained from spleens and mesenteric lymph nodes from Mif − / − mice orally infected with T. gondii had impaired maturation, with decreased expression of CD80, CD86, CD40, and MHC class II [41].…”

Section: Critical Role Of Mif In Toxoplasma Gondii Infectionmentioning

confidence: 99%

“…A recent study using a model of oral T. gondii infection in the BALB/c background also demonstrated an increased lethality and tissue parasitism with reduced IL-12 production and DC activation on Mif − / − mice compared to wild-type mice [41]. DCs obtained from spleens and mesenteric lymph nodes from Mif − / − mice orally infected with T. gondii had impaired maturation, with decreased expression of CD80, CD86, CD40, and MHC class II [41]. Thus, the protective role of MIF in T. gondii infection is apparently related to the production of proinflammatory cytokines, the activation of DC, and the better control of parasite burden.…”

Section: Critical Role Of Mif In Toxoplasma Gondii Infectionmentioning

confidence: 99%