Macrophage Migration Inhibitory Factor (MIF) Promoter Polymorphisms Are Associated With Favorable Hemodynamic Indices In Pulmonary Arterial Hypertension

Author(s):  
Todd M. Kolb ◽  
Danielle Boyce ◽  
Nicholas Rafaels ◽  
Li Gao ◽  
Reda Girgis ◽  
...  
2017 ◽  
Vol 7 (3) ◽  
pp. 730-733 ◽  
Author(s):  
Jeffrey D. Marshall ◽  
Maor Sauler ◽  
Adriano Tonelli ◽  
Youlan Rao ◽  
Richard Bucala ◽  
...  

Macrophage migration inhibitory factor (MIF) and 22 a priori selected biomarkers were measured from pulmonary arterial hypertension (PAH) patients. Significant positive correlations were found between MIF and several angiogenic factors suggesting a possible MIF regulation role in PAH angiogenesis and pathobiology, but simultaneously highlighting the biomarkers profiling complexity in PAH.


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.


2020 ◽  
Vol 9 (9) ◽  
pp. 2936
Author(s):  
Luisa Averdunk ◽  
Jürgen Bernhagen ◽  
Karl Fehnle ◽  
Harald Surowy ◽  
Hermann-Josef Lüdecke ◽  
...  

Background: Macrophage Migration Inhibitory Factor (MIF) is highly elevated after cardiac surgery and impacts the postoperative inflammation. The aim of this study was to analyze whether the polymorphisms CATT5–7 (rs5844572/rs3063368,“-794”) and G>C single-nucleotide polymorphism (rs755622,-173) in the MIF gene promoter are related to postoperative outcome. Methods: In 1116 patients undergoing cardiac surgery, the MIF gene polymorphisms were analyzed and serum MIF was measured by ELISA in 100 patients. Results: Patients with at least one extended repeat allele (CATT7) had a significantly higher risk of acute kidney injury (AKI) compared to others (23% vs. 13%; OR 2.01 (1.40–2.88), p = 0.0001). Carriers of CATT7 were also at higher risk of death (1.8% vs. 0.4%; OR 5.12 (0.99–33.14), p = 0.026). The GC genotype was associated with AKI (20% vs. GG/CC:13%, OR 1.71 (1.20–2.43), p = 0.003). Multivariate analyses identified CATT7 predictive for AKI (OR 2.13 (1.46–3.09), p < 0.001) and death (OR 5.58 (1.29–24.04), p = 0.021). CATT7 was associated with higher serum MIF before surgery (79.2 vs. 50.4 ng/mL, p = 0.008). Conclusion: The CATT7 allele associates with a higher risk of AKI and death after cardiac surgery, which might be related to chronically elevated serum MIF. Polymorphisms in the MIF gene may constitute a predisposition for postoperative complications and the assessment may improve risk stratification and therapeutic guidance.


2003 ◽  
Vol 179 (1) ◽  
pp. 15-23 ◽  
Author(s):  
JA Baugh ◽  
SC Donnelly

The diverse actions of macrophage migration inhibitory factor (MIF) within the immuno-neuroendocrine system are yet to be fully understood, but it is clear that MIF plays a pivotal role in the regulation of both the innate and adaptive immune response. An emerging body of data presently indicates that MIF's position within the cytokine cascade is to act in concert with glucocorticoids to control the 'set point' and magnitude of the immune and inflammatory response. In this article we will review the actions of MIF within the immune system and discuss the overlapping and contrasting aspects of MIF and glucocorticoid biology. In particular we will focus on the role of MIF within the immuno-neuroendocrine interface and suggest molecular mechanisms by which MIF may counter-regulate glucocorticoid function. Finally we will discuss emerging evidence that functional MIF gene-promoter polymorphisms render one susceptible to elevated MIF expression, and the development of an exaggerated immune/inflammatory response that potentiates the progression to chronic inflammatory disease.


2009 ◽  
Vol 200 (4) ◽  
pp. 629-637 ◽  
Author(s):  
Gordon A. Awandare ◽  
Jeremy J. Martinson ◽  
Tom Were ◽  
Collins Ouma ◽  
Gregory C. Davenport ◽  
...  

2019 ◽  
Vol 8 (1) ◽  
Author(s):  
Guillermo Santoscoy‐Ascencio ◽  
Christian Johana Baños‐Hernández ◽  
José Eduardo Navarro‐Zarza ◽  
Jorge Hernández‐Bello ◽  
Richard Bucala ◽  
...  

Cytokine ◽  
2010 ◽  
Vol 51 (2) ◽  
pp. 173-177 ◽  
Author(s):  
Hisakazu Shiroeda ◽  
Tomomitsu Tahara ◽  
Masakatsu Nakamura ◽  
Tomoyuki Shibata ◽  
Tomoe Nomura ◽  
...  

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