scholarly journals Role of the Macrophage Migration Inhibitory Factor in the Pathophysiology of Pre-Eclampsia

2021 ◽  
Vol 22 (4) ◽  
pp. 1823
Author(s):  
Tullia Todros ◽  
Luana Paulesu ◽  
Simona Cardaropoli ◽  
Alessandro Rolfo ◽  
Bianca Masturzo ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Late Onset ◽  
Maternal Serum ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Placental Development ◽  
Major Player

Proinflammatory cytokines are produced in pregnancy in response to the invading pathogens and/or nonmicrobial causes such as damage-associated molecules and embryonic semi-allogenic antigens. While inflammation is essential for a successful pregnancy, an excessive inflammatory response is implicated in several pathologies including pre-eclampsia (PE). This review focuses on the proinflammatory cytokine macrophage migration inhibitory factor (MIF), a critical regulator of the innate immune response and a major player of processes allowing normal placental development. PE is a severe pregnancy-related syndrome characterized by exaggerated inflammatory response and generalized endothelial damage. In some cases, usually of early onset, it originates from a maldevelopment of the placenta, and is associated with intrauterine growth restriction (IUGR) (placental PE). In other cases, usually of late onset, pre-pregnancy maternal diseases represent risk factors for the development of the disease (maternal PE). Available data suggest that low MIF production in early pregnancy could contribute to the abnormal placentation. The resulting placental hypoxia in later pregnancy could produce high release of MIF in maternal serum typical of placental PE. More studies are needed to understand the role of MIF, if any, in maternal PE.

scholarly journals The Role of Macrophage Migration Inhibitory Factor in Alzheimer′s Disease: Conventionally Pathogenetic or Unconventionally Protective?

Molecules ◽  
2020 ◽  
Vol 25 (2) ◽  
pp. 291 ◽  
Author(s):  
Maria Cristina Petralia ◽  
Giuseppe Battaglia ◽  
Valeria Bruno ◽  
Manuela Pennisi ◽  
Katia Mangano ◽  
...  
Keyword(s):  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Late Onset ◽  
Adaptive Immune System ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Adaptive Immune ◽  
Clinical Observations ◽  
Underlying Mechanisms

Recent preclinical and clinical observations have offered relevant insights on the etiopathogenesis of late onset Alzheimer′s disease (AD) and upregulated immunoinflammatory events have been described as underlying mechanisms involved in the development of AD. Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine produced by several cells of the innate and adaptive immune system, as well as non-immune cells. In the present review, we highlight experimental, genetic, and clinical studies on MIF in rodent models of AD and AD patients, and we discuss emerging therapeutic opportunities for tailored modulation of the activity of MIF, that may potentially be applied to AD patients. Dismantling the exact role of MIF and its receptors in AD may offer novel diagnostic and therapeutic opportunities in AD.

scholarly journals Oxygen regulation of macrophage migration inhibitory factor in human placenta

2007 ◽  
Vol 292 (1) ◽  
pp. E272-E280 ◽  
Author(s):  
Francesca Ietta ◽  
Yuanhong Wu ◽  
Roberta Romagnoli ◽  
Nima Soleymanlou ◽  
Barbara Orsini ◽  
...  
Keyword(s):  
High Altitude ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Extravillous Trophoblast ◽  
Macrophage Migration ◽  
Low Oxygen ◽  
Placental Development

Macrophage migration inhibitory factor (MIF) is an important proinflammatory cytokine involved in regulation of macrophage function. In addition, MIF may also play a role in murine and human reproduction. Although both first trimester trophoblast and decidua express MIF, the regulation and functional significance of this cytokine during human placental development remains unclear. We assessed MIF expression throughout normal human placental development, as well as in in vitro (chorionic villous explants) and in vivo (high altitude placentae) models of human placental hypoxia. Dimethyloxalylglycine (DMOG), which stabilizes hypoxia inducible factor-1 under normoxic conditions, was also used to mimic the effects of hypoxia on MIF expression. Quantitative real-time PCR and Western blot analysis showed high MIF protein and mRNA expression at 7–10 wk and lower levels at 11–12 wk until term. Exposure of villous explants to 3% O2 resulted in increased MIF expression and secretion relative to standard conditions (20% O2). DMOG treatment under 20% O2 increased MIF expression. In situ hybridization and immunohistochemistry showed elevated MIF expression in low oxygen-induced extravillous trophoblast cells. Finally, a significant increase in MIF transcript was observed in placental tissues from high-altitude pregnancies. Hence, three experimental models of placental hypoxia (early gestation, DMOG treatment, and high altitude) converge in stimulating increased MIF, supporting the conclusion that placental-derived MIF is an oxygen-responsive cytokine highly expressed in physiological in vivo and in in vitro low oxygen conditions.

scholarly journals Role of Macrophage Migration Inhibitory Factor in the Regulatory T Cell Response of Tumor-Bearing Mice

2012 ◽  
Vol 189 (8) ◽  
pp. 3905-3913 ◽  
Author(s):  
Susanna Choi ◽  
Hang-Rae Kim ◽  
Lin Leng ◽  
Insoo Kang ◽  
William L. Jorgensen ◽  
...  
Keyword(s):  
T Cell ◽  
Migration Inhibitory Factor ◽  
Regulatory T Cell ◽  
Cell Response ◽  
Macrophage Migration Inhibitory Factor ◽  
T Cell Response ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Tumor Bearing

scholarly journals The role of human macrophage migration inhibitory factor in promoting angiogenesis

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
XiYong Yu ◽  
ZhiXin Shan ◽  
QiuXiong Lin ◽  
ShiXia Cai ◽  
Min Yang ◽  
...  
Keyword(s):  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Human Macrophage ◽  
Macrophage Migration

Role of macrophage migration inhibitory factor in bleomycin-induced lung injury and fibrosis in mice

2002 ◽  
Vol 283 (1) ◽  
pp. L156-L162 ◽  
Author(s):  
Yoshinori Tanino ◽  
Hironi Makita ◽  
Kenji Miyamoto ◽  
Tomoko Betsuyaku ◽  
Yoshinori Ohtsuka ◽  
...  
Keyword(s):  
Lung Injury ◽  
Migration Inhibitory Factor ◽  
Lung Fibrosis ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Lung Injury Score ◽  
Macrophage Migration ◽  
Acute Lung Inflammation ◽  
Intratracheal Administration

Macrophage migration inhibitory factor (MIF) is a unique cytokine that reportedly overrides the anti-inflammatory effect of endogenous glucocorticoids. MIF has been demonstrated to be involved in a variety of inflammatory diseases. In this study, we examined the role of MIF in bleomycin (BLM)-induced lung injury and fibrosis. The levels of MIF in lung tissues and bronchoalveolar lavage fluids were significantly increased in the period 5–10 days after intratracheal administration of BLM. Treatment with the anti-MIF antibody significantly reduced the mortality at 14 days and the histopathological lung injury score at 10 days. These effects were accompanied with significant suppression of the accumulation of inflammatory cells in the alveolar space and tumor necrosis factor-α in the lungs at 7 days. However, the anti-MIF antibody did not affect either the content of lung hydroxyproline or the histopathological lung fibrosis score at 21 days after BLM. These data provide further evidence for the crucial role of MIF in acute lung inflammation but do not support the involvement of MIF in lung fibrosis induced by BLM in mice.

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