scholarly journals Macrophage migration inhibitory factor activates the inflammatory response in joint capsule fibroblasts following post-traumatic joint contracture

Aging ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 5804-5823
Author(s):  
Yuxin Zhang ◽  
Shenji Lu ◽  
Shuai Fan ◽  
Lili Xu ◽  
Xin Jiang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Joint Capsule ◽  
Joint Contracture ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Post Traumatic

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 Macrophage Migration Inhibitory Factor Regulates Joint Capsule Fibrosis by Promoting TGF-β1 Production in Fibroblasts

2020 ◽  
Author(s):  
Yuxin Zhang ◽  
Shenji Lu ◽  
Kexin Wang ◽  
Shuai Fan ◽  
Lili Xu ◽  
...  
Keyword(s):  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Transforming Growth Factor ◽  
Membrane Surface ◽  
Joint Capsule ◽  
Inhibitory Factor ◽  
Mitogen Activated Protein Kinase ◽  
Specific Cell ◽  
Macrophage Migration ◽  
Tgf Β1

Abstract Background: Joint capsule fibrosis caused by excessive inflammation results in post-traumatic joint contracture (PTJC). Transforming growth factor (TGF)-β1 plays a key role in PTJC by regulating fibroblast functions, however, cytokine-induced TGF-β1 expression in specific cell types remains poorly characterized. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine involved in inflammation- and fibrosis-associated pathophysiology. Results: In this study, we investigated whether MIF can facilitate TGF-β1 production from fibroblasts and regulate joint capsule fibrosis following PTJC. Our data demonstrated that MIF and TGF-β1 significantly increased in fibroblasts of injured rat posterior joint capsules. Treatment the lesion sites with MIF inhibitor 4-Iodo-6-phenylpyrimidine (4-IPP) reduced TGF-β1 production and relieved joint capsule inflammation and fibrosis. In vitro, MIF facilitated TGF-β1 expression in primary joint capsule fibroblasts by activating mitogen-activated protein kinase (MAPK) (P38, ERK) signaling through coupling with membrane surface receptor CD74, which in turn affected fibroblast functions and promoted MIF production. Conclusion: Our results reveal a novel function of trauma-induced MIF in the occurrence and development of joint capsule fibrosis. Further investigation of the underlying mechanism may provide potential therapeutic targets for PTJC.

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