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 ◽  
...  

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.

2021 ◽  
Vol 22 (4) ◽  
pp. 1823
Author(s):  
Tullia Todros ◽  
Luana Paulesu ◽  
Simona Cardaropoli ◽  
Alessandro Rolfo ◽  
Bianca Masturzo ◽  
...  

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.


2012 ◽  
Vol 189 (8) ◽  
pp. 3905-3913 ◽  
Author(s):  
Susanna Choi ◽  
Hang-Rae Kim ◽  
Lin Leng ◽  
Insoo Kang ◽  
William L. Jorgensen ◽  
...  

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
XiYong Yu ◽  
ZhiXin Shan ◽  
QiuXiong Lin ◽  
ShiXia Cai ◽  
Min Yang ◽  
...  

2002 ◽  
Vol 283 (1) ◽  
pp. L156-L162 ◽  
Author(s):  
Yoshinori Tanino ◽  
Hironi Makita ◽  
Kenji Miyamoto ◽  
Tomoko Betsuyaku ◽  
Yoshinori Ohtsuka ◽  
...  

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.


2018 ◽  
Vol 2018 (2) ◽  
Author(s):  
Mohamed Ahmed ◽  
Edmund Miller

Macrophage migration inhibitory factor (MIF) has been described as a pro-inflammatory cytokine and regulator of neuro-endocrine function. It plays an important upstream role in the inflammatory cascade by promoting the release of other inflammatory cytokines such as TNF-alpha and IL-6, ultimately triggering a chronic inflammatory immune response. As lungs can synthesize and release MIF, many studies have investigated the potential role of MIF as a biomarker in assessment of patients with pulmonary arterial hypertension (PAH) and using anti-MIFs as a new therapeutic modality for PAH.


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