scholarly journals Increased Plasma Concentration of Macrophage Migration Inhibitory Factor (MIF) and MIF mRNA in Mononuclear Cells in the Obese and the Suppressive Action of Metformin

2004 ◽  
Vol 89 (10) ◽  
pp. 5043-5047 ◽  
Author(s):  
Paresh Dandona ◽  
Ahmad Aljada ◽  
Husam Ghanim ◽  
Priya Mohanty ◽  
Chandana Tripathy ◽  
...  
Keyword(s):  
Plasma Concentration ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Mononuclear Cells ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Suppressive Action

scholarly journals Immunohistological Characterization of Macrophage Migration Inhibitory Factor Expression in Plasmodium falciparum-Infected Placentas

2005 ◽  
Vol 73 (6) ◽  
pp. 3287-3293 ◽  
Author(s):  
Sujittra Chaisavaneeyakorn ◽  
Naomi Lucchi ◽  
Carlos Abramowsky ◽  
Caroline Othoro ◽  
Sansanee C. Chaiyaroj ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Mononuclear Cells ◽  
Placental Malaria ◽  
Inhibitory Factor ◽  
Immunoperoxidase Staining ◽  
Macrophage Migration ◽  
Human Trophoblast ◽  
Hofbauer Cells

ABSTRACT Previously, we have shown that macrophage migration inhibitory factor (MIF) was highly elevated in the placental intervillous blood (IVB) of Plasmodium falciparum-infected women. Here, we compared the expression of MIF in placental tissues obtained from P. falciparum-infected and -uninfected women. Immunoperoxidase staining showed a consistent pattern of MIF expression in syncytiotrophoblasts, extravillous trophoblasts, IVB mononuclear cells, and amniotic epithelial cells, irrespective of their malaria infection status. Cytotrophoblast, villous stroma, and Hofbauer cells showed focal staining. Only amniotic epithelial and IVB mononuclear cells from P. falciparum-infected placentas exhibited significantly higher level of MIF expression than uninfected placentas. Stimulation of syncytilized human trophoblast BeWo cells with P. falciparum-infected erythrocytes that were selected to bind these cells resulted in significant increases in MIF secretion, whereas control erythrocytes, lipopolysaccharides, and synthetic β-hematin had minimal effect. These findings suggest that placental malaria modulates MIF expression in different placental compartments.

scholarly journals Individual responsiveness of macrophage migration inhibitory factor predicts long-term cognitive impairment after bacterial meningitis

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Anne T. Kloek ◽  
Mercedes Valls Seron ◽  
Ben Schmand ◽  
Michael W. T. Tanck ◽  
Arie van der Ende ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Bacterial Meningitis ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Pneumococcal Meningitis ◽  
Mononuclear Cells ◽  
Ex Vivo ◽  
Inhibitory Factor ◽  
Macrophage Migration

Abstract Background Patients with pneumococcal meningitis are at risk for death and neurological sequelae including cognitive impairment. Functional genetic polymorphisms of macrophage migration inhibitory factor (MIF) alleles have shown to predict mortality of pneumococcal meningitis. Methods We investigated whether MIF concentrations during the acute phase of disease were predictive for death in a nationwide prospective cohort study. Subsequently, we studied whether individual ex vivo MIF response years after meningitis was associated with the development of cognitive impairment. Results We found that in the acute illness of pneumococcal meningitis, higher plasma MIF concentrations were predictive for mortality (p = 0.009). Cognitive impairment, examined 1–5 years after meningitis, was present in 11 of 79 patients after pneumococcal meningitis (14%), as compared to 1 of 63 (2%) in controls, and was consistently associated with individual variability in MIF production by peripheral blood mononuclear cells after ex vivo stimulation with various infectious stimuli. Conclusions Our study confirms the role of MIF in poor disease outcome of pneumococcal meningitis. Inter-individual differences in MIF production were associated with long-term cognitive impairment years after pneumococcal meningitis. The present study provides evidence that MIF mediates long-term cognitive impairment in bacterial meningitis survivors and suggests a potential role for MIF as a target of immune-modulating adjunctive therapy.

scholarly journals A critical role for the host mediator macrophage migration inhibitory factor in the pathogenesis of malarial anemia

2006 ◽  
Vol 203 (5) ◽  
pp. 1185-1196 ◽  
Author(s):  
Michael A. McDevitt ◽  
Jianlin Xie ◽  
Shanmugasundaram Ganapathy-Kanniappan ◽  
Jason Griffith ◽  
Aihua Liu ◽  
...  
Keyword(s):  
Migration Inhibitory Factor ◽  
Malaria Infection ◽  
Macrophage Migration Inhibitory Factor ◽  
Mononuclear Cells ◽  
Critical Role ◽  
Inhibitory Factor ◽  
Mitogen Activated Protein Kinase ◽  
Macrophage Migration ◽  
Erythroid Progenitor ◽  
Malarial Anemia

The pathogenesis of malarial anemia is multifactorial, and the mechanisms responsible for its high mortality are poorly understood. Studies indicate that host mediators produced during malaria infection may suppress erythroid progenitor development (Miller, K.L., J.C. Schooley, K.L. Smith, B. Kullgren, L.J. Mahlmann, and P.H. Silverman. 1989. Exp. Hematol. 17:379–385; Yap, G.S., and M.M. Stevenson. 1991. Ann. NY Acad. Sci. 628:279–281). We describe an intrinsic role for macrophage migration inhibitory factor (MIF) in the development of the anemic complications and bone marrow suppression that are associated with malaria infection. At concentrations found in the circulation of malaria-infected patients, MIF suppressed erythropoietin-dependent erythroid colony formation. MIF synergized with tumor necrosis factor and γ interferon, which are known antagonists of hematopoiesis, even when these cytokines were present in subinhibitory concentrations. MIF inhibited erythroid differentiation and hemoglobin production, and it antagonized the pattern of mitogen-activated protein kinase phosphorylation that normally occurs during erythroid progenitor differentiation. Infection of MIF knockout mice with Plasmodium chabaudi resulted in less severe anemia, improved erythroid progenitor development, and increased survival compared with wild-type controls. We also found that human mononuclear cells carrying highly expressed MIF alleles produced more MIF when stimulated with the malarial product hemozoin compared with cells carrying low expression MIF alleles. These data suggest that polymorphisms at the MIF locus may influence the levels of MIF produced in the innate response to malaria infection and the likelihood of anemic complications.

Macrophage migration inhibitory factor of the parasitic nematode Trichinella spiralis

2001 ◽  
Vol 357 (2) ◽  
pp. 373-383 ◽  
Author(s):  
Timothy H. P. TAN ◽  
Steve A. V. EDGERTON ◽  
Rashmi KUMARI ◽  
Mark S. B. McALISTER ◽  
S. Mark ROWE ◽  
...  
Keyword(s):  
Methyl Ester ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Mononuclear Cells ◽  
Quaternary Structure ◽  
Trichinella Spiralis ◽  
Human Peripheral Blood ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Filarial Nematodes

cDNAs were obtained for macrophage migration-inhibitory factor (MIF)/l-dopachrome methyl ester tautomerase homologues from the parasitic nematodes Trichinella spiralis (TsMIF) and Trichuris trichiura (TtMIF). The translated sequences, which were partly confirmed by sequencing of proteolytic fragments, show 42 and 44% identity respectively with human or mouse MIF, and are shorter by one C-terminal residue. Unlike vertebrate MIF and MIF homologues of filarial nematodes, neither TsMIF nor TtMIF contain cysteine residues. Soluble recombinant TsMIF, expressed in Escherichia coli showed secondary structure (by CD spectroscopy) and quaternary structure (by light-scattering and gel filtration) similar to that of the trimeric mammalian MIFs and d-dopachrome tautomerase. The catalytic specificity of recombinant TsMIF in the ketonization of phenylpyruvate (1.4×106M−1·s−1) was comparable with that of human MIF, while that of p-hydroxyphenylpyruvate (9.1×104M−1·s−1) was 71-fold lower. TsMIF showed high specificity in tautomerization of the methyl ester of l-dopachrome compared with non-esterified l-dopachrome (>87000-fold) and a high kcat (≈ 4×104s−1). The crystal structure, determined to 1.65 Å (1 Å = 0.1nm), was generally similar to that of human MIF, but differed in the boundaries of the putative active-site pocket, which can explain the low activity towards p-hydroxyphenylpyruvate. The central pore was blocked, but was continuous, with the three putative tautomerase sites. Recombinant TsMIF (5ng/ml–5pg/ml) inhibited migration of human peripheral-blood mononuclear cells in a manner similar to that shown by human MIF, but had no effect from 5 to 500ng/ml on anti-CD3-stimulated murine T-cell proliferation. TsMIF was detected in supernatants of T. spiralis larvae cultured in vitro at 6ng/ml (55ng/mg total secreted protein). In conclusion TsMIF has structural, catalytic and cell-migration-inhibitory properties which indicate that it is partially orthologous to mammalian MIF.

287: Macrophage Migration Inhibitory Factor and its Receptor CD74 are Upregulated in the Urothelium of Interstitial Cystitis Patients

2006 ◽  
Vol 175 (4S) ◽  
pp. 95-96 ◽  
Author(s):  
Pedro L. Vera ◽  
Kenneth A. lczkowski ◽  
Robert M. Moldwin ◽  
Leslie Kushner ◽  
Katherine L. Meyer-Siegler
Keyword(s):  
Interstitial Cystitis ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration
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