Macrophage migration inhibitory factor in lung tissue of idiopathic pulmonary fibrosis patients

Abstract

In conclusion, MIF is a pleiotropic cytokine involved in the pathogenesis of IPF being mainly expressed in the areas of remodeling and active fibrosis, in bronchiolar and alveolar epithelium, and in the peripheral zone of fibroblastic foci.

Predictive potential of macrophage migration inhibitory factor (MIF) in patients with heart failure with preserved ejection fraction (HFpEF)

“…Beyond this background, MIF seems to be a good candidate marker to be evaluated in HFpEF since it was shown to be a marker for oxidative stress, organ fibrosis, cell damage, atherosclerosis, lung disease, rheumatic diseases, sepsis [ 21 ], severe illness, and chronic kidney disease [ 12 , 13 , 18 , 19 , 22 – 25 ]. MIF is a pleiotropic upstream pro-inflammatory integral mediator of the innate immune system, stimulating the release of multiple cytokines, including tumor necrosis factor (TNF)-α which has been shown to activate matrix metalloproteinases and to be responsible for collagen degradation and progressive left ventricular dilation [ 26 ].…”

“…MIF is quasi-ubiquitously expressed and stored in numerous cell types, while specifically secreted from the pituitary gland upon endotoxaemia [ 9 ], from immune cells upon inflammatory stimulation, as well as from selected endothelial and parenchymal cells upon hypoxic, hyperoxic, and other stress stimuli [ 10 ]. MIF is a well-established mediator of a number of acute and chronic inflammatory diseases including atherosclerosis, chronic kidney disease, organ fibrosis, and rheumatoid arthritis [ 11 – 13 ]. MIF’s role in cardiovascular disease is dual, as it also has a clear-cut cardioprotective role in the setting of myocardial ischemia and reperfusion (I/R) injury, contrasting the bonafide negative function in the promotion of arteriosclerosis development [ 14 ].…”

Macrophage migration inhibitory factor (MIF) in the development and progression of pulmonary arterial hypertension

“…There are also several chronic inflammatory lung-associated pathologies that have been noted to be associated with changes in MIF. In particular, in idiopathic pulmonary fibrosis there is increased MIF expression in areas of remodeling, bronchiolar and alveolar epithelium, and ongoing fibrosis 71,72 . In systemic sclerosis, where MIF may be involved in the amplifying proinflammatory loop leading to scleroderma tissue remodeling 73 , an MIF promoter polymorphism is associated with susceptibility to pulmonary arterial hypertension in diffuse cutaneous systemic sclerosis (SSc) 74 .…”

Macrophage migration inhibitory factor contributes to the pathogenesis of benign lymphoepithelial lesion of the lacrimal gland

“…MIF promotes cell proliferation and migration by interacting with its proposed receptors cluster of differentiation 74 (CD74), C-X-C chemokine receptor 2 (CXCR2), CXCR4, and CXCR7 [ 13 , 16 – 19 ], which may trigger the activation of several pathways, including mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/Akt pathways, facilitating the activation of transcription factors required for the expression of pro-inflammatory cytokines and cell cycle regulators, for cell migration, proliferation, and survival [ 13 , 16 – 19 ]. Recently, MIF has also been linked to several fibrotic diseases, including liver [ 20 , 21 ], kidney [ 22 , 23 ], lung, [ 24 , 25 ], and bladder [ 26 ] fibrosis. Although MIF has both pro-fibrotic [ 23 , 26 – 28 ] and anti-fibrotic [ 22 , 29 ] activities, the precise mechanisms of these functions in fibrosis remain unclear.…”