Macrophage migration inhibitory factor is a critical mediator of systemic inflammatory response syndrome

2001 ◽  
Vol 27 (7) ◽  
pp. 1187-1193 ◽  
Author(s):  
S. Gando ◽  
J. Nishihira ◽  
S. Kobayashi ◽  
Y. Morimoto ◽  
S. Nanzaki ◽  
...  
Keyword(s):  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Systemic Inflammatory Response ◽  
Inhibitory Factor ◽  
Macrophage Migration

scholarly journals Macrophage migration inhibitory factor: a neuroendocrine modulator of chronic inflammation

2003 ◽  
Vol 179 (1) ◽  
pp. 15-23 ◽  
Author(s):  
JA Baugh ◽  
SC Donnelly
Keyword(s):  
Inflammatory Response ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Molecular Mechanisms ◽  
Adaptive Immune Response ◽  
Gene Promoter ◽  
Chronic Inflammatory Disease ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Promoter Polymorphisms

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.

scholarly journals Adrenomedullin Is Both Proinflammatory and Antiinflammatory: Its Effects on Gene Expression and Secretion of Cytokines and Macrophage Migration Inhibitory Factor in NR8383 Macrophage Cell Line

Endocrinology ◽  
2005 ◽  
Vol 146 (3) ◽  
pp. 1321-1327 ◽  
Author(s):  
Louisa Y. F. Wong ◽  
Bernard M. Y. Cheung ◽  
Yuk-Yin Li ◽  
Fai Tang
Keyword(s):  
Inflammatory Response ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Culture Media ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Macrophage Cell ◽  
Gene Expressions ◽  
Initiation And Propagation ◽  
Tnf Α

Adrenomedullin (ADM) is a potent vasorelaxant peptide that plays important roles in cardiovascular homeostasis and inflammatory response. ADM derived from macrophages is one of the major sources of ADM that is produced in the inflammatory process. To assess the functions of ADM in inflammation, we studied the temporal changes in ADM production and its effect on secretion of macrophage migration inhibitory factor (MIF) and cytokine response of NR8383 rat macrophages activated by lipopolysaccharide (LPS). NR8383 cells were stimulated by LPS in the absence and presence of exogenous ADM, and the concentrations of ADM, MIF, and proinflammatory cytokines (IL-6, TNF-α, and IL-1β) in the culture media and gene expressions of the cells were measured. We confirmed that the secretion and mRNA expression of ADM in the macrophages were markedly increased by LPS. ADM increased initial secretion of MIF and IL-1β from both nonstimulated and LPS-stimulated cells, and it also increased basal and LPS-induced IL-6 secretion of the cells by 2- to 15-fold. However, it reduced secretion of TNF-α from LPS-stimulated cells by 34–56%. Our results suggest that ADM modulates MIF secretion and cytokine production and plays important roles in both the initiation and propagation of the inflammatory response.

scholarly journals Macrophage Migration Inhibitory Factor Is Enhanced in Acute Coronary Syndromes and Is Associated with the Inflammatory Response

PLoS ONE ◽  
2012 ◽  
Vol 7 (6) ◽  
pp. e38376 ◽  
Author(s):  
Iris I. Müller ◽  
Karin A. L. Müller ◽  
Heiko Schönleber ◽  
Athanasios Karathanos ◽  
Martina Schneider ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Migration Inhibitory Factor ◽  
Acute Coronary Syndromes ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Coronary Syndromes

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.

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