scholarly journals A genetic role for macrophage migration inhibitory factor (MIF) in Epinephelus awoara infected with Vibrio parahaemolyticus

2016 ◽  
Vol 14 (3) ◽  
pp. 184-189
Author(s):  
Xiaojin Xu ◽  
Benhong Sang ◽  
Gang Luo
Keyword(s):  
Migration Inhibitory Factor ◽  
Vibrio Parahaemolyticus ◽  
Macrophage Migration Inhibitory Factor ◽  
Head Kidney ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Mrna Levels ◽  
Tissue Levels ◽  
Tnf Α ◽  
Epinephelus Awoara

Macrophage migration inhibitory factor (MIF) is a key pro-inflammatory cytokine in immuno-inflammatory diseases. For the first time, we examined the expression of MIF in Epinephelus awoara ( E. awoara). MIF expressions have been detected in the head kidney, spleen, liver, brain, intestine, gill, heart, stomach, and muscle of E. awoara infected with Vibrio parahaemolyticus. The mRNA levels observed in infected groupers were higher than those in healthy groupers. MIF, tumor necrosis factor-α (TNF-α), and interleukin-1 (IL-1) tissue levels have been measured by ELISA. A significant increase in MIF, TNF-α, and IL-1 tissue levels have been found in the treatment groups compared with those in controls. MIF, TNF-α and IL-1 tissue levels in the spleen, head kidney, intestine, and liver of E. awoara during the challenge trial with V. parahaemolyticus were significantly higher than those in controls. There was evidence of functions of MIF in a positive feedback loop with TNF-α and IL-1 that could perpetuate the inflammatory process in grouper infected with V. parahaemolyticus. In conclusion, these results indicated that MIF was related to pathogen-induced immune response.

scholarly journals Role of Macrophage Migration Inhibitory Factor in Otitis Media with Effusion in Adults

2003 ◽  
Vol 10 (3) ◽  
pp. 417-422 ◽  
Author(s):  
Shin Kariya ◽  
Mitsuhiro Okano ◽  
Katsuya Aoji ◽  
Michiya Kosaka ◽  
Emiko Chikumoto ◽  
...  
Keyword(s):  
Otitis Media ◽  
Middle Ear ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Otitis Media With Effusion ◽  
Fluid Collection ◽  
Inhibitory Factor ◽  
Enzyme Linked Immunosorbent Assay ◽  
Macrophage Migration ◽  
Tnf Α

ABSTRACT Otitis media with effusion (OME) is one of the most common ear diseases. Bacterial endotoxins and several inflammatory cytokines appear to be involved in the pathogenesis of OME in children; however, little is known of the immunological aspects of the onset of OME in adults. We sought to determine the presence of macrophage migration inhibitory factor (MIF) as well as interleukin 1β (IL-1β), tumor necrosis factor alpha (TNF-α), RANTES (regulated upon activation, normal T-cell expressed and presumably secreted), and endotoxin in middle ear effusions (MEEs) from adult patients with OME. In addition, the levels of MIF in MEEs from adults and children were compared. MEE was obtained from 95 adults and 11 children. The levels of MIF, IL-1β, TNF-α, and RANTES were determined by enzyme-linked immunosorbent assay, and the concentrations of endotoxin and total protein were determined by the Endospec assay and bicinchoninic acid assay, respectively. MIF was detected in 97.9% of the MEEs from adults, while endotoxin, IL-1β, TNF-α, and RANTES were detected in 96.8, 12.6, 5.3, and 43.9%, respectively. In addition, the level of MIF was significantly higher than those of endotoxin, IL-1β, and TNF-α. A positive correlation between the levels of MIF and endotoxin was observed. MIF and endotoxin were detected in 81.8 and 72.7%, respectively, of the MEEs from the children. The level of MIF was significantly higher in the children, and conversely that of endotoxin was significantly higher in the adults. These results suggest that the interaction between MIF and endotoxin may promote fluid collection in the middle ear, particularly in adults.

scholarly journals Knockdown of Macrophage Migration Inhibitory Factor Disrupts Adipogenesis in 3T3-L1 Cells

Endocrinology ◽  
2008 ◽  
Vol 149 (12) ◽  
pp. 6037-6042 ◽  
Author(s):  
Daisuke Ikeda ◽  
Shinji Sakaue ◽  
Mitsunori Kamigaki ◽  
Hiroshi Ohira ◽  
Naofumi Itoh ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Clonal Expansion ◽  
Cell Number ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Mrna Levels ◽  
Transfected Cells ◽  
Mitotic Clonal Expansion

Obesity is a condition in which adipose tissue mass is expanded. Increases in both adipocyte size and number contribute to enlargement of adipose tissue. The increase in cell number is thought to be caused by proliferation and differentiation of preadipocytes. Macrophage migration inhibitory factor (MIF) is expressed in adipocytes, and intracellular MIF content is increased during adipogenesis. Therefore, we hypothesized that MIF is associated with adipocyte biology during adipogenesis and focused on the influence of MIF on adipogenesis. To examine the effects of MIF on adipocytes, MIF expression in 3T3-L1 preadipocytes was inhibited by RNA interference, and cell differentiation was induced by standard procedures. The triglyceride content of MIF small interfering RNA (siRNA)-transfected 3T3-L1 cells was smaller than that of nonspecific siRNA-transfected cells. In addition, MIF knockdown apparently abrogated increases in adiponectin mRNA levels during differentiation. Gene expression of peroxisome proliferator-activated receptor (PPAR)γ, CCAAT/enhancer binding protein (C/EBP)α, and C/EBPδ decreased with MIF siRNA transfection, but C/EBPβ expression increased. Cell number and incorporation of 5-bromo-2-deoxyuridine into cells decreased from 1–3 d and from 14–20 h, respectively, after induction of differentiation in MIF siRNA-transfected cells, thus suggesting that MIF siRNA inhibits mitotic clonal expansion. Taken together, these results indicated that MIF regulates differentiation of 3T3-L1 preadipocytes, at least partially, through inhibition of mitotic clonal expansion and/or C/EBPδ expression.

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.

Null mutation in macrophage migration inhibitory factor prevents muscle cell loss and fibrosis in partial bladder outlet obstruction

2006 ◽  
Vol 291 (6) ◽  
pp. F1343-F1353 ◽  
Author(s):  
John A. Taylor ◽  
Qing Zhu ◽  
Brian Irwin ◽  
Yazeed Maghaydah ◽  
John Tsimikas ◽  
...  
Keyword(s):  
Migration Inhibitory Factor ◽  
Bladder Outlet Obstruction ◽  
Macrophage Migration Inhibitory Factor ◽  
Outlet Obstruction ◽  
Inhibitory Factor ◽  
Detrusor Muscle ◽  
Detrusor Underactivity ◽  
Macrophage Migration ◽  
Mrna Levels ◽  
Partial Bladder Outlet Obstruction

Idiopathic detrusor underactivity (DU) and detrusor decompensation which develops following partial bladder outlet obstruction (pBOO) are both associated with smooth muscle degeneration and fibrosis. Macrophage migration inhibitory factor (MIF), an important mediator of bladder inflammation, has been shown to promote fibroblast survival and muscle death in other tissues. We evaluated the hypothesis that MIF has similar actions in the bladder by studying detrusor responses to pBOO or sham surgery in anesthetized female mice rendered null for the mif gene (MIF KO) and in wild-type (WT) controls, all killed 3 wk after surgery. WT mice revealed intense MIF immunoreactivity in urothelial cells which decreased, without change in overall mif mRNA levels. Stereologically sound quantitative morphometric measurements were performed in the middetrusor region of each bladder. MIF KO bladders were normal in appearance, yet were 30–40% heavier, with increased middetrusor collagen and muscle, compared with WT controls. In WT mice, pBOO increased the collagen-to-muscle ratio 1.9-fold and middetrusor collagen 1.8-fold, while nucleated muscle counts were 22% lower. In MIF KO mice, by contrast, pBOO had no significant effect on any of these parameters. In primary bladder muscle cultures, treatment with rMIF protein increased TUNEL staining, raising the proportion of early and late apoptotic cells on flow cytometry. Our studies implicate MIF in the sequence of events leading to detrusor muscle loss and fibrosis in obstruction. They raise the possibility that strategies designed to antagonize MIF synthesis, release, or biological activity could prevent or delay DU and urinary retention.

Macrophage migration inhibitory factor is a cardiac-derived myocardial depressant factor

2003 ◽  
Vol 285 (6) ◽  
pp. H2500-H2509 ◽  
Author(s):  
Leslie B. Garner ◽  
Monte S. Willis ◽  
Deborah L. Carlson ◽  
J. Michael DiMaio ◽  
Michael D. White ◽  
...  
Keyword(s):  
Migration Inhibitory Factor ◽  
Cardiac Dysfunction ◽  
Macrophage Migration Inhibitory Factor ◽  
Left Ventricular ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Mrna Levels ◽  
Western Blots ◽  
Endotoxin Challenge ◽  
Lps Challenge

Macrophage migration inhibitory factor (MIF) is a pluripotent proinflammatory cytokine that is ubiquitously expressed in organs, including the heart. However, no specific role for MIF in modulating cardiac performance has yet been described. Therefore, we examined cardiac MIF expression in mice after LPS challenge (4 mg/kg) and tested the hypothesis that MIF is a mediator of LPS-induced cardiac dysfunction. Western blots of whole heart lysates, as well as immunohistochemistry, documented constitutive MIF protein expression in the heart. Cardiac MIF protein levels significantly decreased after LPS challenge, reaching a nadir at 12 h, and then returned to baseline by 24 h. This pattern was consistent with MIF release from cytoplasmic stores after endotoxin challenge. After release of protein, MIF mRNA levels increased 24–48 h postchallenge. To determine the functional consequences of MIF release, we treated LPS-challenged mice with anti-MIF neutralizing antibodies or isotype control antibodies. Anti-MIF-treated animals had significantly improved cardiac function, as evidenced by a significant improvement in left ventricular (LV) fractional shortening percentage at 8, 12, 24, and 48 h after endotoxin challenge. In support of these findings, perfusion of isolated beating mouse hearts (Langendorff preparation) with recombinant MIF (20 ng/ml) led to a significant decrease in both systolic and diastolic performance [LV pressure (LVP), positive and negative first derivative of LVP with respect to time, and rate of LVP rise at developed pressure of 40 mmHg]. This study demonstrates that MIF mediates LPS-induced cardiac dysfunction and suggests that MIF should be considered a pharmacological target for the treatment of cardiac dysfunction in sepsis and potentially other cardiac diseases.

scholarly journals The Macrophage Migration Inhibitory Factor Homolog of Entamoeba histolytica Binds to and Immunomodulates Host Macrophages

2014 ◽  
Vol 82 (9) ◽  
pp. 3523-3530 ◽  
Author(s):  
Shannon N. Moonah ◽  
Mayuresh M. Abhyankar ◽  
Rashidul Haque ◽  
William A. Petri
Keyword(s):  
Entamoeba Histolytica ◽  
Migration Inhibitory Factor ◽  
Tissue Damage ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Content Type ◽  
Amebic Colitis ◽  
Tnf Α ◽  
Wide Range

ABSTRACTThe host inflammatory response contributes to the tissue damage that occurs during amebic colitis, with tumor necrosis factor alpha (TNF-α) being a key mediator of the gut inflammation observed. Mammalian macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that plays an important role in the exacerbation of a wide range of inflammatory diseases, including colitis. We identified a MIF gene homolog in theEntamoeba histolyticagenome, raising the question of whetherE. histolyticaMIF (EhMIF) has proinflammatory activity similar to that of mammalian MIF. In this report, we describe the first functional characterization ofEhMIF. Antibodies were prepared against recombinantly expressedEhMIF and used to demonstrate thatEhMIF is expressed as a 12-kDa protein localized to the cytoplasm of trophozoites. In a manner similar to that of mammalian MIF,EhMIF interacted with the MIF receptor CD74 and bound to macrophages.EhMIF induced interleukin-6 (IL-6) production. In addition,EhMIF enhanced TNF-α secretion by amplifying TNF-α production by lipopolysaccharide (LPS)-stimulated macrophages and by inhibiting the glucocorticoid-mediated suppression of TNF-α secretion.EhMIF was expressed during human infection, as evidenced by the presence of anti-EhMIF antibodies in the sera of children living in an area whereE. histolyticainfection is endemic. Anti-EhMIF antibodies did not cross-react with human MIF. The ability ofEhMIF to modulate host macrophage function may promote an exaggerated proinflammatory immune response and contribute to the tissue damage seen in amebic colitis.

scholarly journals Tissue-specific regulation of inflammation by macrophage migration inhibitory factor and glucocorticoids in fructose-fed Wistar rats

2013 ◽  
Vol 110 (3) ◽  
pp. 456-465 ◽  
Author(s):  
Nataša Veličković ◽  
Ana Djordjevic ◽  
Ana Vasiljević ◽  
Biljana Bursać ◽  
Danijela Vojnović Milutinović ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Mrna Expression ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Metabolic Inflammation ◽  
High Fructose Diet ◽  
High Fructose ◽  
Tnf Α

High fructose consumption is commonly associated with insulin resistance, disturbed glucose homeostasis and low-grade inflammation. Increased glucocorticoid production within adipose tissue has been implicated in the pathogenesis of fructose-induced metabolic syndrome. Immunosuppressive actions of glucocorticoids can be counter-regulated by macrophage migration inhibitory factor (MIF), which is recognised as a key molecule in metabolic inflammation. In the present study, we hypothesised that coordinated action of glucocorticoids and MIF can mediate the effects of a high-fructose diet on adipose tissue and liver inflammation. We examined the effects of long-term consumption of a 10 % fructose solution on corticosterone (CORT) and MIF levels in rat blood plasma, liver and adipose tissue, as well as MIF and TNF-α mRNA expression and NF-κB activation in the same tissues. The high-fructose diet led to an increase in both CORT and MIF in the adipose tissue, and a highly significant positive correlation between their levels was observed. The attenuated NF-κB activation and unaltered TNF-α mRNA expression noticed in the adipose tissue could be interpreted as an outcome of the opposing actions of CORT and MIF. In contrast to adipose tissue, inflammation in the liver was characterised by NF-κB activation, an increased TNF-α mRNA level and unchanged levels of MIF protein, MIF mRNA and CORT. Overall, these findings suggest that a high-fructose diet differently affects the levels of glucocorticoids and MIF in the adipose tissue and liver, implicating that fructose over-consumption has tissue-specific effects on regulation of metabolic inflammation.

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