The Experts below are selected from a list of 303 Experts worldwide ranked by ideXlab platform
Richard Bucala - One of the best experts on this subject based on the ideXlab platform.
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Abstract 15796: Downregulation of the Macrophage Migration Inhibitory Factor Pathway in Advanced Heart Failure
Circulation, 2018Co-Authors: Kenneth Bedi, Richard Bucala, Lin Leng, Kenneth B. Margulies, Lawrence YoungAbstract:Background: Macrophage Migration Inhibitory Factor (MIF) and its homolog D-dopachrome tautomerase (DDT) are cytokines highly expressed in cardiomyocytes and have autocrine-paracrine effects, signal...
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Benzisothiazolones as modulators of macrophage Migration Inhibitory Factor.
Bioorganic & medicinal chemistry letters, 2011Co-Authors: William L. Jorgensen, Lin Leng, Alexander Trofimov, Alissa A. Hare, Richard BucalaAbstract:Substituted N-phenylbenzisothiazolones have been investigated as inhibitors of the tautomerase activity of the proinflammatory cytokine MIF (macrophage Migration Inhibitory Factor). Numerous compounds were found to possess antagonist activity in the low micromolar range with the most potent being the 6-hydroxy analog 1w. Compound 1w and the p-cyano analog 1c were also shown to exhibit significant inhibition of the binding of MIF to its transmembrane receptor CD74. Consistently, both compounds were also found to retard the MIF-dependent phosphorylation of ERK1/2 in human synovial fibroblasts.
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the macrophage Migration Inhibitory Factor glucocorticoid dyad regulation of inflammation and immunity
Molecular Endocrinology, 2007Co-Authors: Harry Flaster, Jürgen Bernhagen, Thierry Calandra, Richard BucalaAbstract:The cytokine macrophage Migration Inhibitory Factor (MIF) occupies a unique position in physiology by its ability to directly regulate the immunosuppressive actions of glucocorticoids. We review herein the interactions between MIF and glucocorticoids within the immune system and discuss the relevance of the MIF-glucocorticoid regulatory dyad in physiology and immunopathology. Therapeutic antagonism of MIF may be an effective approach for steroid-sparing therapies in patients with refractory autoimmune or inflammatory diseases.
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macrophage Migration Inhibitory Factor a probable link between inflammation and cancer
Immunity, 2007Co-Authors: Richard Bucala, Seamas C. DonnellyAbstract:The pleiotropic effects of macrophage Migration Inhibitory Factor (MIF) place it in a central position in the immunopathogenesis of many diseases. Here we discuss the current understanding of MIF's role and highlight it as a potential link between inflammatory activation and malignant progression.
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Sex steroid regulation of macrophage Migration Inhibitory Factor in normal and inflamed colon in the female rat
Gastroenterology, 2007Co-Authors: Eric Houdeau, Richard Bucala, Lin Leng, Raphaël Moriez, Mathilde Leveque, Christel Cartier, Aurelie Waget, Lionel Bueno, Jean FioramontiAbstract:Sex steroid regulation of macrophage Migration Inhibitory Factor in normal and inflamed colon in the female rat
Christian P Speer - One of the best experts on this subject based on the ideXlab platform.
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Systemic fetal inflammation and reduced concentrations of macrophage Migration Inhibitory Factor in tracheobronchial aspirate fluid of extremely premature infants.
American journal of obstetrics and gynecology, 2008Co-Authors: Wolfgang Thomas, Silvia Seidenspinner, Natalia Kawczyńska-leda, Boris W Kramer, Maria Chmielnicka-kopaczyk, Alexander Marx, Marta Szymankiewicz, Christian P SpeerAbstract:Macrophage Migration Inhibitory Factor is a proinflammatory mediator of innate immunity, enhances cell growth, and plays a role in preterm delivery. We speculated that funisitis, reflecting fetal systemic inflammation, would be associated with higher concentrations of macrophage Migration Inhibitory Factor in airways of extremely premature infants. We measured macrophage Migration Inhibitory Factor by enzyme linked immunosorbent assay in tracheobronchial aspirate fluid of 35 ventilated infants less than 30 weeks' gestational age, throughout the first week of life. Three groups were distinguished histologically: chorioamnionitis, funisitis, and control. Unexpectedly, funisitis was associated with significantly decreased macrophage Migration Inhibitory Factor in tracheobronchial aspirate fluid on day 1 (P < .01) and levels remained lower than in the chorioamnionitis group thereafter. For the 35 patients in total, macrophage Migration Inhibitory Factor steadily declined. Decreased macrophage Migration Inhibitory Factor concentrations in airways of extremely premature infants with systemic fetal inflammation early in life might predispose them to pulmonary infection and interfere with maturation of the lung, contributing to adverse pulmonary outcome.
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Systemic fetal inflammation and reduced concentrations of macrophage Migration Inhibitory Factor in tracheobronchial aspirate fluid of extremely premature infants.
American Journal of Obstetrics and Gynecology, 2007Co-Authors: Wolfgang Thomas, Silvia Seidenspinner, Natalia Kawczyńska-leda, Boris W Kramer, Maria Chmielnicka-kopaczyk, Alexander Marx, Marta Szymankiewicz, Christian P SpeerAbstract:Objective Macrophage Migration Inhibitory Factor is a proinflammatory mediator of innate immunity, enhances cell growth, and plays a role in preterm delivery. We speculated that funisitis, reflecting fetal systemic inflammation, would be associated with higher concentrations of macrophage Migration Inhibitory Factor in airways of extremely premature infants. Study Design We measured macrophage Migration Inhibitory Factor by enzyme linked immunosorbent assay in tracheobronchial aspirate fluid of 35 ventilated infants less than 30 weeks' gestational age, throughout the first week of life. Three groups were distinguished histologically: chorioamnionitis, funisitis, and control. Results Unexpectedly, funisitis was associated with significantly decreased macrophage Migration Inhibitory Factor in tracheobronchial aspirate fluid on day 1 ( P Conclusion Decreased macrophage Migration Inhibitory Factor concentrations in airways of extremely premature infants with systemic fetal inflammation early in life might predispose them to pulmonary infection and interfere with maturation of the lung, contributing to adverse pulmonary outcome.
Poul Thorsen - One of the best experts on this subject based on the ideXlab platform.
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Serum macrophage Migration Inhibitory Factor in the prediction of preterm delivery.
American journal of obstetrics and gynecology, 2008Co-Authors: Brad D Pearce, Sicily E Garvin, Jakob Grove, Elizabeth A Bonney, Donald J Dudley, Diana E Schendel, Poul ThorsenAbstract:Macrophage Migration Inhibitory Factor is a soluble mediator that helps govern the interaction between cytokines and stress hormones (eg, cortisol). We determined whether maternal macrophage Migration Inhibitory Factor levels predicted subsequent preterm delivery. A nested case-control study measuring serum macrophage Migration Inhibitory Factor concentration at 9-23 weeks' gestation in women who ultimately delivered preterm (n = 60) compared with control women who delivered at term (n = 122). We also examined the connection of macrophage Migration Inhibitory Factor with self-reported psychosocial variables. Macrophage Migration Inhibitory Factor was elevated in the preterm delivery cases (P = .0004), and log macrophage Migration Inhibitory Factor concentration showed a graded response relationship with likelihood of preterm delivery. High-macrophage Migration Inhibitory Factor was also associated with maternal risk-taking behavior, which itself was a risk Factor for preterm delivery. Macrophage Migration Inhibitory Factor remained associated independently with preterm delivery after adjusting regression models for several other preterm delivery risk Factors (odds ratio, 3.11, 95% confidence interval, 1.54-6.30). High-serum macrophage Migration Inhibitory concentration in early to midpregnancy is linked with subsequent preterm delivery.
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Serum macrophage Migration Inhibitory Factor in the prediction of preterm delivery.
American Journal of Obstetrics and Gynecology, 2008Co-Authors: Brad D Pearce, Sicily E Garvin, Jakob Grove, Elizabeth A Bonney, Donald J Dudley, Diana Schendel, Poul ThorsenAbstract:Objective Macrophage Migration Inhibitory Factor is a soluble mediator that helps govern the interaction between cytokines and stress hormones (eg, cortisol). We determined whether maternal macrophage Migration Inhibitory Factor levels predicted subsequent preterm delivery. Study Design A nested case-control study measuring serum macrophage Migration Inhibitory Factor concentration at 9-23 weeks' gestation in women who ultimately delivered preterm (n = 60) compared with control women who delivered at term (n = 122). We also examined the connection of macrophage Migration Inhibitory Factor with self-reported psychosocial variables. Results Macrophage Migration Inhibitory Factor was elevated in the preterm delivery cases ( P = .0004), and log macrophage Migration Inhibitory Factor concentration showed a graded response relationship with likelihood of preterm delivery. High-macrophage Migration Inhibitory Factor was also associated with maternal risk-taking behavior, which itself was a risk Factor for preterm delivery. Macrophage Migration Inhibitory Factor remained associated independently with preterm delivery after adjusting regression models for several other preterm delivery risk Factors (odds ratio, 3.11, 95% confidence interval, 1.54-6.30). Conclusion High-serum macrophage Migration Inhibitory concentration in early to midpregnancy is linked with subsequent preterm delivery.
Lin Leng - One of the best experts on this subject based on the ideXlab platform.
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Abstract 15796: Downregulation of the Macrophage Migration Inhibitory Factor Pathway in Advanced Heart Failure
Circulation, 2018Co-Authors: Kenneth Bedi, Richard Bucala, Lin Leng, Kenneth B. Margulies, Lawrence YoungAbstract:Background: Macrophage Migration Inhibitory Factor (MIF) and its homolog D-dopachrome tautomerase (DDT) are cytokines highly expressed in cardiomyocytes and have autocrine-paracrine effects, signal...
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Benzisothiazolones as modulators of macrophage Migration Inhibitory Factor.
Bioorganic & medicinal chemistry letters, 2011Co-Authors: William L. Jorgensen, Lin Leng, Alexander Trofimov, Alissa A. Hare, Richard BucalaAbstract:Substituted N-phenylbenzisothiazolones have been investigated as inhibitors of the tautomerase activity of the proinflammatory cytokine MIF (macrophage Migration Inhibitory Factor). Numerous compounds were found to possess antagonist activity in the low micromolar range with the most potent being the 6-hydroxy analog 1w. Compound 1w and the p-cyano analog 1c were also shown to exhibit significant inhibition of the binding of MIF to its transmembrane receptor CD74. Consistently, both compounds were also found to retard the MIF-dependent phosphorylation of ERK1/2 in human synovial fibroblasts.
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Sex steroid regulation of macrophage Migration Inhibitory Factor in normal and inflamed colon in the female rat
Gastroenterology, 2007Co-Authors: Eric Houdeau, Richard Bucala, Lin Leng, Raphaël Moriez, Mathilde Leveque, Christel Cartier, Aurelie Waget, Lionel Bueno, Jean FioramontiAbstract:Sex steroid regulation of macrophage Migration Inhibitory Factor in normal and inflamed colon in the female rat
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Macrophage Migration Inhibitory Factor.
Critical Care Medicine, 2005Co-Authors: Lin Leng, Richard BucalaAbstract:Macrophage Migration Inhibitory Factor (MIF) has been proposed to be the physiologic counter-regulator of glucocorticoid action within the immune system. In this role, MIF's position within the cytokine cascade is to act in concert with glucocorticoids to control both the "set point" and the magnitude of the inflammatory response. As well as overriding the immunosuppressive effects of glucocorticoids, it is now well established that MIF has a direct proinflammatory role in inflammatory diseases, such as sepsis, rheumatoid arthritis, and glomerulonephritis. The functions of MIF within the immune system are both unique and diverse, and although a unified molecular mechanism of action remains to be elucidated, there have been significant advances in our understanding of how MIF affects cellular processes. This review discusses the pathogenic role of MIF in inflammatory disease and highlights the novel structural, functional, and mechanistic properties of MIF.
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Macrophage Migration Inhibitory Factor increases neuronal delayed rectifier K+ current.
Journal of neurophysiology, 2005Co-Authors: Tomokazu Matsuura, Richard Bucala, Lin Leng, Chengwen Sun, Aphrodite Kapurniotu, Jürgen Bernhagen, Anatoly E. Martynyuk, Colin SumnersAbstract:Macrophage Migration Inhibitory Factor (MIF) has widespread actions in the immune, endocrine, and nervous systems. Previously, we reported that increases in the intracellular levels of MIF depress ...
Wolfgang Thomas - One of the best experts on this subject based on the ideXlab platform.
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Systemic fetal inflammation and reduced concentrations of macrophage Migration Inhibitory Factor in tracheobronchial aspirate fluid of extremely premature infants.
American journal of obstetrics and gynecology, 2008Co-Authors: Wolfgang Thomas, Silvia Seidenspinner, Natalia Kawczyńska-leda, Boris W Kramer, Maria Chmielnicka-kopaczyk, Alexander Marx, Marta Szymankiewicz, Christian P SpeerAbstract:Macrophage Migration Inhibitory Factor is a proinflammatory mediator of innate immunity, enhances cell growth, and plays a role in preterm delivery. We speculated that funisitis, reflecting fetal systemic inflammation, would be associated with higher concentrations of macrophage Migration Inhibitory Factor in airways of extremely premature infants. We measured macrophage Migration Inhibitory Factor by enzyme linked immunosorbent assay in tracheobronchial aspirate fluid of 35 ventilated infants less than 30 weeks' gestational age, throughout the first week of life. Three groups were distinguished histologically: chorioamnionitis, funisitis, and control. Unexpectedly, funisitis was associated with significantly decreased macrophage Migration Inhibitory Factor in tracheobronchial aspirate fluid on day 1 (P < .01) and levels remained lower than in the chorioamnionitis group thereafter. For the 35 patients in total, macrophage Migration Inhibitory Factor steadily declined. Decreased macrophage Migration Inhibitory Factor concentrations in airways of extremely premature infants with systemic fetal inflammation early in life might predispose them to pulmonary infection and interfere with maturation of the lung, contributing to adverse pulmonary outcome.
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Systemic fetal inflammation and reduced concentrations of macrophage Migration Inhibitory Factor in tracheobronchial aspirate fluid of extremely premature infants.
American Journal of Obstetrics and Gynecology, 2007Co-Authors: Wolfgang Thomas, Silvia Seidenspinner, Natalia Kawczyńska-leda, Boris W Kramer, Maria Chmielnicka-kopaczyk, Alexander Marx, Marta Szymankiewicz, Christian P SpeerAbstract:Objective Macrophage Migration Inhibitory Factor is a proinflammatory mediator of innate immunity, enhances cell growth, and plays a role in preterm delivery. We speculated that funisitis, reflecting fetal systemic inflammation, would be associated with higher concentrations of macrophage Migration Inhibitory Factor in airways of extremely premature infants. Study Design We measured macrophage Migration Inhibitory Factor by enzyme linked immunosorbent assay in tracheobronchial aspirate fluid of 35 ventilated infants less than 30 weeks' gestational age, throughout the first week of life. Three groups were distinguished histologically: chorioamnionitis, funisitis, and control. Results Unexpectedly, funisitis was associated with significantly decreased macrophage Migration Inhibitory Factor in tracheobronchial aspirate fluid on day 1 ( P Conclusion Decreased macrophage Migration Inhibitory Factor concentrations in airways of extremely premature infants with systemic fetal inflammation early in life might predispose them to pulmonary infection and interfere with maturation of the lung, contributing to adverse pulmonary outcome.