Review: Putative roles for the macrophage migratory inhibitory factor at the maternal fetal interface

Bevilacqua, Estela Maris Andrade Forell; Paulesu, Luana; Ferro, Eloísa Amália Vieira; Ietta, Francesca; Faria, Miriam R.; Lorenzon-Ojea, Aline R.; Costa, Ana Luiza Fontes de Azevedo; Martucci, Mariane Ferracin

doi:10.1016/j.placenta.2013.10.015

Cited by 21 publications

(16 citation statements)

References 54 publications

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“…MIF expression levels are increased in peritoneal macrophages and endometriotic lesions [13] , [14] and its concentrations are elevated in the peritoneal fluid [16] . MIF may play an important role in the retention of activated peritoneal macrophages [46] , stimulation of endometrial cell adhesion [22] , induction of angiogenic phenotype in ectopic endometrial cells [11] , up-regulation of MMP activity [43] and promotion of cell survival [40] , [47] , [48] .…”

Section: Discussionmentioning

confidence: 99%

Macrophage Migration Inhibitory Factor Is Involved in Ectopic Endometrial Tissue Growth and Peritoneal-Endometrial Tissue Interaction In Vivo: A Plausible Link to Endometriosis Development

et al. 2014

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Pelvic inflammation is a hallmark of endometriosis pathogenesis and a major cause of the disease's symptoms. Abnormal immune and inflammatory changes may not only contribute to endometriosis-major symptoms, but also contribute to ectopic endometrial tissue growth and endometriosis development. A major pro-inflammatory factors found elevated in peritoneal fluid of women with endometriosis and to be overexpressed in peritoneal fluid macrophages and active, highly vascularized and early stage endometriotic lesions, macrophage migration inhibitory factor (MIF) appeared to induce angiogenic and inflammatory and estrogen producing phenotypes in endometriotic cells in vitro and to be a possible therapeutic target in vivo. Using a mouse model where MIF-knock out (KO) mice received intra-peritoneal injection of endometrial tissue from MIF-KO or syngeneic wild type (WT) mice and vice versa, our current study revealed that MIF genetic depletion resulted in a marked reduction ectopic endometrial tissue growth, a disrupted tissue structure and a significant down regulation of the expression of major inflammatory (cyclooxygenease-2), cell adhesion (αv and β3 integrins), survival (B-cell lymphoma-2) and angiogenic (vascular endothelial cell growth) factorsrelevant to endometriosis pathogenesis, whereas MIF add-back to MIF-KO mice significantly restored endometriosis-like lesions number and size. Interestingly, cross-experiments revealed that MIF presence in both endometrial and peritoneal host tissues is required for ectopic endometrial tissue growth and pointed to its involvement in endometrial-peritoneal interactions. This study provides compelling evidence for the role of MIF in endometriosis development and its possible interest for a targeted treatment of endometriosis.

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Section: Discussionmentioning

confidence: 99%

Macrophage Migration Inhibitory Factor Is Involved in Ectopic Endometrial Tissue Growth and Peritoneal-Endometrial Tissue Interaction In Vivo: A Plausible Link to Endometriosis Development

et al. 2014

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“…Additionally, congenital toxoplasmosis can induce abortion and preterm labor, depending on the gestational age when infection occurs ( Robbins et al, 2012 ). Our group has investigated the role of MIF in congenital toxoplasmosis, since MIF is constitutively expressed during pregnancy and possibly associated with the physiology of gestation ( Bevilacqua et al, 2014 ). Additionally, MIF plays an important role in the host defense against infection by parasites ( Rosado and Rodriguez-Sosa, 2001 ).…”

Section: Discussionmentioning

confidence: 99%

“…MIF is a multifunctional proinflammatory cytokine that was first described as a factor produced by lymphocytes associated with inhibition of random macrophage migration during delayed hypersensitivity responses ( Bloom and Bennett, 1966 ; David, 1966 ). Concerning pregnancy, MIF was described as a factor produced at implantation sites and is mostly expressed by trophoblast cells, presenting a putative role in pregnancy physiology ( Bevilacqua et al, 2014 ). An earlier study by our group, using human placental explants, demonstrated that MIF and its receptor (CD74) were upregulated in response to T. gondii infection, thus playing an important role in controlling infection in a gestational age-dependent manner ( de Oliveira Gomes et al, 2011 ).…”

Section: Introductionmentioning

confidence: 99%

Macrophage Migration Inhibitory Factor (MIF) Prevents Maternal Death, but Contributes to Poor Fetal Outcome During Congenital Toxoplasmosis

et al. 2018

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Migration inhibitory factor (MIF) is a pro-inflammatory cytokine that plays important roles in physiology, pathology, immunology and parasitology, including the control of infection by protozoa parasites such as Toxoplasma gondii. As the MIF function in congenital toxoplasmosis is not fully elucidated yet, the present study brings new insights for T. gondii infection in the absence of MIF based on pregnant C57BL/6MIF-/- mouse models. Pregnant C57BL/6MIF-/- and C57BL/6WT mice were infected with 05 cysts of T. gondii (ME49 strain) on the first day of pregnancy (dop) and were euthanized at 8 dop. Non-pregnant and non-infected females were used as control. Our results demonstrated that MIF-/- mice have more accentuated change in body weight and succumbed to infection first than their WT counterparts. Otherwise, pregnancy outcome was less destructive in MIF-/- mice compared to WT ones, and the former had an increase in the mast cell recruitment and IDO expression and consequently presented less inflammatory cytokine production. Also, MIF receptor (CD74) was upregulated in MIF-/- mice, indicating that a compensatory mechanism may be required in this model of study. The global absence of MIF was associated with attenuation of pathology in congenital toxoplasmosis, but resulted in female death probably because of uncontrolled infection. Altogether, ours results demonstrated that part of the immune response that protects a pregnant female from T. gondii infection, favors fetal damage.

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“…Despite the number of studies on MIF in pregnancy 16 , 17 , only little is known about its role at the maternal-foetal interface. It has been demonstrated that trophoblast MIF reduces the cytotoxicity of human decidual NK cells 18 .…”

Section: Introductionmentioning

confidence: 99%

Role of the Macrophage Migration Inhibitory Factor (MIF) in the survival of first trimester human placenta under induced stress conditions

Ietta

Ferro

Bevilacqua

et al. 2018

Sci Rep

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Macrophage Migration Inhibitory Factor (MIF) is a multifunctional molecule highly secreted by human placenta mainly in the early phases of pregnancy. Studies in different cells show that MIF is a pro-survival factor by binding to its receptor CD74. By using the in vitro model of placental explants from first trimester pregnancy, we investigated the role of MIF in the survival of placental cells under induced stress conditions that promote apoptosis or mimic the hypoxia/re-oxygenation (H/R) injury that placenta could suffer in vivo. We demonstrated that recombinant MIF (rMIF) treatment was able to reduce caspase-3 activation when cultures were challenged with the apoptosis-inducer Carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP) while, in the cultures exposed to H/R, the treatment with rMIF did not show any effect. However, a significant increase in caspase-3 and caspase-8 activation was found when H/R-exposed cultures, were treated with anti-MIF or anti-CD74 antibody. We also observed that under H/R, a significant amount of endogenous MIF was released into the medium, which could account for the lack of effect of rMIF added to the cultures. Our results demonstrate for the first time that the MIF/CD74 axis contributes to maintain trophoblast homeostasis, by preventing abnormal apoptotic death.

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Review: Putative roles for the macrophage migratory inhibitory factor at the maternal fetal interface

Cited by 21 publications

References 54 publications

Macrophage Migration Inhibitory Factor Is Involved in Ectopic Endometrial Tissue Growth and Peritoneal-Endometrial Tissue Interaction In Vivo: A Plausible Link to Endometriosis Development

Macrophage Migration Inhibitory Factor Is Involved in Ectopic Endometrial Tissue Growth and Peritoneal-Endometrial Tissue Interaction In Vivo: A Plausible Link to Endometriosis Development

Macrophage Migration Inhibitory Factor (MIF) Prevents Maternal Death, but Contributes to Poor Fetal Outcome During Congenital Toxoplasmosis

Role of the Macrophage Migration Inhibitory Factor (MIF) in the survival of first trimester human placenta under induced stress conditions

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