Research Topics
Genomes and Genes | Pranoti MandrekarSummaryAffiliation: University of Massachusetts Medical School Country: USA Publications
Research Grants
| Collaborators
|
Detail Information
Publications
The opposite effects of acute and chronic alcohol on lipopolysaccharide-induced inflammation are linked to IRAK-M in human monocytesPranoti Mandrekar
University of Massachusetts Medical School, Department of Medicine, Worcester, MA 01605, USA
J Immunol 183:1320-7. 2009..Our data indicate that IRAK-M is a central player in the opposite regulation of LPS signaling by different lengths of alcohol exposure in monocytes...
Signalling pathways in alcohol-induced liver inflammationPranoti Mandrekar
Department of Medicine, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
J Hepatol 50:1258-66. 2009..In this review we describe the key signalling intermediates leading to alcohol-induced inflammation in alcoholic liver disease...
Signaling mechanisms in alcoholic liver injury: role of transcription factors, kinases and heat shock proteinsPranoti Mandrekar
Liver Center, Department of Medicine, University of Massachusetts Medical School, LRB 213, 364 Plantation Street, Worcester, MA 01605 2324, USA
World J Gastroenterol 13:4979-85. 2007....- Alcohol exposure regulates heat shock transcription factor binding and heat shock proteins 70 and 90 in monocytes and macrophages: implication for TNF-alpha regulationPranoti Mandrekar
Department of Medicine, University of Massachusetts Medical Center, Worcester, Massachusetts 01605, USA
J Leukoc Biol 84:1335-45. 2008..These results suggest that alcohol exposure differentially regulates hsp70 and hsp90 via HSF-1 activation. Further, hsp90 regulates TNF-alpha production in macrophages contributing to alcohol-induced inflammation... - Inhibition of NF-kappa B binding correlates with increased nuclear glucocorticoid receptor levels in acute alcohol-treated human monocytesPranoti Mandrekar
Division of Gastroenterology, Department of Medicine, University of Massachusetts Medical School, Worcester 01605, USA
Alcohol Clin Exp Res 26:1872-9. 2002..Here, we show for the first time that acute alcohol (25 mM) exposure modulates GR activation in monocytes... - Epigenetic regulation in alcoholic liver diseasePranoti Mandrekar
Department of Medicine, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, United States
World J Gastroenterol 17:2456-64. 2011..Finally, the role of alcohol-mediated oxidative stress in epigenetic regulation in ALD is described. A better understanding of these mechanisms is crucial for designing novel epigenetic based therapies to ameliorate ALD... - An essential role for monocyte chemoattractant protein-1 in alcoholic liver injury: regulation of proinflammatory cytokines and hepatic steatosis in micePranoti Mandrekar
Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
Hepatology 54:2185-97. 2011.... - The critical role of toll-like receptor (TLR) 4 in alcoholic liver disease is independent of the common TLR adapter MyD88Istvan Hritz
Department of Medicine, University of Massachusetts Medical School, University of Massachusetts, Worcester, MA 01605, USA
Hepatology 48:1224-31. 2008..These results suggest that the common TLR adapter, MyD88, is dispensable in TLR4-mediated liver injury in ALD... - Viral and host factors induce macrophage activation and loss of toll-like receptor tolerance in chronic HCV infectionAngela Dolganiuc
University of Massachusetts Medical School, Worcester, Massachusetts, USA
Gastroenterology 133:1627-36. 2007..Persistent inflammation contributes to progression of liver damage in chronic HCV (cHCV) infection. Repeated exposure to toll-like receptor (TLR) ligands results in tolerance, a protective mechanism aimed at limiting inflammation... - MicroRNA expression profile in Lieber-DeCarli diet-induced alcoholic and methionine choline deficient diet-induced nonalcoholic steatohepatitis models in miceAngela Dolganiuc
Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605 2324, USA
Alcohol Clin Exp Res 33:1704-10. 2009..Each miRNA controls the expression of multiple targets; miRNAs have been linked to regulation of lipid metabolism and inflammation... - Increased lipopolysaccharide sensitivity in alcoholic fatty livers is independent of leptin deficiency and toll-like receptor 4 (TLR4) or TLR2 mRNA expressionLaszlo Romics
Liver Center, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01606, USA
Alcohol Clin Exp Res 29:1018-26. 2005..CONCLUSION: These results imply that the increased sensitivity of AFL to LPS occurs without up-regulation of TLR2 or TLR4 genes and may be related to an imbalance of pro-inflammatory/oxidative and cytoprotective mechanisms... - Deficiency in myeloid differentiation factor-2 and toll-like receptor 4 expression attenuates nonalcoholic steatohepatitis and fibrosis in miceTimea Csak
Department of Medicine, University of Massachusetts, Medical School, Worcester, 01605 2324, USA
Am J Physiol Gastrointest Liver Physiol 300:G433-41. 2011..In conclusion, our results demonstrate a novel, critical role for LPS recognition complex, including MD-2 and TLR4, through NADPH activation in liver steatosis, and fibrosis in a NASH model in mice... - Interferon regulatory factor 3 and type I interferons are protective in alcoholic liver injury in mice by way of crosstalk of parenchymal and myeloid cellsJan Petrasek
Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
Hepatology 53:649-60. 2011..These results suggest potential therapeutic targets in ALD... - Bone marrow-derived immune cells mediate sensitization to liver injury in a myeloid differentiation factor 88-dependent fashionIstvan Hritz
Department of Medicine, University of Massachusetts, Medical School, Worcester, MA 01605 2324, USA
Hepatology 48:1342-7. 2008..These results demonstrate that MyD88 in immune cells rather than in liver parenchymal cells plays an important role in inflammatory cell recruitment and liver injury... - Diverse regulation of NF-kappaB and peroxisome proliferator-activated receptors in murine nonalcoholic fatty liverLaszlo Romics
Liver Center, Division of Gastroenterology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605-2324, USA
Hepatology 40:376-85. 2004..Thus, an imbalance between PPAR-mediated anti-inflammatory and NF-kappaB-mediated proinflammatory signals may contribute to increased inflammation in the fatty liver... - Toll-like receptor 2 mediates inflammatory cytokine induction but not sensitization for liver injury by Propioni- bacterium acnesLaszlo Romics
Liver Center, Department of Medicine, University of Massachusetts Medical School, LRB 215, 364 Plantation Street, Worcester, MA 01605 2324, USA
J Leukoc Biol 78:1255-64. 2005..These results suggest that although P. acnes triggers TLR2-mediated cell activation, TLR2-independent but MyD88-dependent mechanisms mediate in vivo sensitization by P. acnes for LPS-induced liver injury... - Acute alcohol activates STAT3, AP-1, and Sp-1 transcription factors via the family of Src kinases to promote IL-10 production in human monocytesOxana Norkina
University of Massachusetts Medical School, Department of Medicine, LRB 215, 364 Plantation Street, Worcester, MA 01605, USA
J Leukoc Biol 82:752-62. 2007..Our data suggest that acute alcohol activates Src/STAT3 and Src/MAPK/STAT3, AP-1, and Sp-1 pathways as important mechanisms for IL-10-mediated immunomodulation after acute alcohol use... - Acute alcohol intake induces SOCS1 and SOCS3 and inhibits cytokine-induced STAT1 and STAT3 signaling in human monocytesOxana Norkina
Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
Alcohol Clin Exp Res 32:1565-73. 2008..Here we aimed to explore the effect of acute alcohol on induction of SOCS1/SOCS3 and regulation of STAT3/STAT1 pathways induced by IL-6 or IFNs in human monocytes... - Selective priming to Toll-like receptor 4 (TLR4), not TLR2, ligands by P. acnes involves up-regulation of MD-2 in miceLaszlo Romics
Liver Center, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
Hepatology 40:555-64. 2004..In conclusion, P. acnes priming to selective TLR4-mediated liver injury is associated with up-regulation of TLR4 and MD-2 and is likely to involve IFN-gamma and prevent TLR4 desensitization by P. acnes... - Additive inhibition of dendritic cell allostimulatory capacity by alcohol and hepatitis C is not restored by DC maturation and involves abnormal IL-10 and IL-2 inductionAngela Dolganiuc
Department of Medicine, University of Massachusetts Medical School, Worcester, 01605-2324, USA
Alcohol Clin Exp Res 27:1023-31. 2003..HCV and alcohol interact to modulate innate and adaptive immune responses via dendritic cells... - Critical role of toll-like receptors and the common TLR adaptor, MyD88, in induction of granulomas and liver injuryArumugam Velayudham
Liver Center, Department of Medicine, University of Massachusetts Medical School, Plantation Street, Worcester, MA 01605, USA
J Hepatol 45:813-24. 2006..Toll-like receptors (TLR) recognize pathogens and regulate innate immune activation. Here, we investigated the roles of TLR9 and the common TLR adaptor, MyD88, in liver injury... - Hepatitis C virus core and nonstructural protein 3 proteins induce pro- and anti-inflammatory cytokines and inhibit dendritic cell differentiationAngela Dolganiuc
Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
J Immunol 170:5615-24. 2003..Our results reveal that HCV core and NS3 proteins activate monocytes and inhibit DC differentiation in the absence of the intact virus and mediate some of the immunoinhibitory effects of HCV via IL-10 induction... - Up-regulation of microRNA-155 in macrophages contributes to increased tumor necrosis factor {alpha} (TNF{alpha}) production via increased mRNA half-life in alcoholic liver diseaseShashi Bala
Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
J Biol Chem 286:1436-44. 2011..In conclusion, our novel data demonstrate that chronic alcohol consumption increases miR-155 in macrophages via NF-κB and the increased miR-155 contributes to alcohol-induced elevation in TNFα production via increased mRNA stability... - TLR2- and TLR4-mediated signals determine attenuation or augmentation of inflammation by acute alcohol in monocytesShilpa Oak
Liver Center, Division of Gastroenterology, Department of Medicine, University of Massachusetts Medical School, Worcester, 01605, USA
J Immunol 176:7628-35. 2006..Thus, the complexity of TLR-mediated signals may determine attenuation or augmentation of inflammatory responses by acute alcohol... - Acute alcohol exposure exerts anti-inflammatory effects by inhibiting IkappaB kinase activity and p65 phosphorylation in human monocytesPranoti Mandrekar
Department of Medicine, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
J Immunol 178:7686-93. 2007..These findings further implicate an important role for IKKbeta in the acute effects of alcohol in immune cells... - Inhibition of myeloid dendritic cell accessory cell function and induction of T cell anergy by alcohol correlates with decreased IL-12 productionPranoti Mandrekar
Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
J Immunol 173:3398-407. 2004..Taken together, alcohol both in vitro and in vivo can impair generation of Th1 immune responses via inhibition of DC differentiation and accessory cell function through mechanisms that involve decreased IL-12 induction... - Moderate alcohol intake in humans attenuates monocyte inflammatory responses: inhibition of nuclear regulatory factor kappa B and induction of interleukin 10Pranoti Mandrekar
Department of Medicine, University of Massachusetts Medical Center, Worcester, MA 01605, USA
Alcohol Clin Exp Res 30:135-9. 2006..These mechanisms may contribute to the beneficial effects of moderate alcohol use on atherosclerosis... - Human monocytes, macrophages, and dendritic cells: alcohol treatment methodsGyongyi Szabo
Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA
Methods Mol Biol 447:113-24. 2008..Here, we summarize the different effects of acute and chronic alcohol on monocyte, macrophage, and dendritic cell functions in humans and describe methods for separation and functional evaluation of these cell types... - Modulation of non-alcoholic steatohepatitis by pattern recognition receptors in mice: the role of toll-like receptors 2 and 4Gyongyi Szabo
Liver Center, Division of Gastroenterology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
Alcohol Clin Exp Res 29:140S-145S. 2005..These results demonstrate that TLR2 deficiency results in increased liver injury in association with nonalcoholic steatohepatitis and may suggest a protective role for TLR2-mediated signals in liver injury... - Heme oxygenase-1 mediates the anti-inflammatory effects of acute alcohol on IL-10 induction involving p38 MAPK activation in monocytesYvonne Drechsler
Department of Medicine, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
J Immunol 177:2592-600. 2006..Thus, HO-1 activation is a key mediator of the anti-inflammatory effects of acute alcohol on monocytes... - Hepatocyte-specific hypoxia-inducible factor-1α is a determinant of lipid accumulation and liver injury in alcohol-induced steatosis in miceBharath Nath
Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA
Hepatology 53:1526-37. 2011..The alcohol-induced chemokine MCP-1 triggers lipid accumulation in hepatocytes via HIF-1α activation, suggesting a mechanistic link between inflammation and hepatic steatosis in alcoholic liver disease... - VSL#3 probiotic treatment attenuates fibrosis without changes in steatohepatitis in a diet-induced nonalcoholic steatohepatitis model in miceArumugam Velayudham
Department of Medicine, Liver Center, University of Massachusetts Medical School, Worcester, MA 01605 2324, USA
Hepatology 49:989-97. 2009..The mechanisms of VSL#3-mediated protection from MCD diet-induced liver fibrosis likely include modulation of collagen expression and impaired TGFbeta signaling... - Hepatitis C virus (HCV) core protein-induced, monocyte-mediated mechanisms of reduced IFN-alpha and plasmacytoid dendritic cell loss in chronic HCV infectionAngela Dolganiuc
University of Massachusetts Medical School, Department of Medicine, Worcester, MA 01605, USA
J Immunol 177:6758-68. 2006..These mechanisms are likely to contribute to HCV viral escape from immune responses... - Effect of ethanol on inflammatory responses. Implications for pancreatitisGyongyi Szabo
Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA
Pancreatology 7:115-23. 2007..Alcohol use alters inflammatory cell responses. While alcohol has direct effects on pancreatic acinar cells, activation of inflammatory cells is a major component of the pathology of alcoholic pancreatitis... - Ethanol-mediated regulation of transcription factors in immunocompetent cellsGyongyi Szabo
Department of Medicine, University of Massachusetts Medical School, LRB 215, 364 Plantation Street, Worcester, MA 01605 2324, USA
Front Biosci 7:a80-9. 2002.... - RSA 2004: combined basic research satellite symposium - session four: hepatitis virus and alcohol interactions in immunity and liver diseaseGyongyi Szabo
University of Massachusetts Medical Center, Department of Medicine, Worcester, MA 01605-2324, USA
Alcohol Clin Exp Res 29:1753-7. 2005.... - Inhibition of antigen-presenting cell functions by alcohol: implications for hepatitis C virus infectionGyongyi Szabo
Liver Center, Division of Gastroenterology, University of Massachusetts Medical School LRB215, 364 Plantation Street, Worcester, MA 01604, USA
Alcohol 33:241-9. 2004.... - Inhibition of heat shock protein (molecular weight 90 kDa) attenuates proinflammatory cytokines and prevents lipopolysaccharide-induced liver injury in miceAditya Ambade
Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
Hepatology 55:1585-95. 2012..Our results suggest a novel application for 17-DMAG in alleviating LPS-induced liver injury... - Acute ethanol treatment modulates Toll-like receptor-4 association with lipid raftsAngela Dolganiuc
Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605-2324, USA
Alcohol Clin Exp Res 30:76-85. 2006..We propose that alcohol-induced effects on lipid rafts may contribute to modulation of TLR4-CD14-triggered early cellular responses... - Innate immune response and hepatic inflammationGyongyi Szabo
Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
Semin Liver Dis 27:339-50. 2007..The specificity of Toll-like receptors and the mechanisms of innate immune cell activation are discussed in relation to acute and chronic liver injury including viral, alcoholic, nonalcoholic, and drug-induced hepatitis... - RSA 2004: combined basic research satellite symposium-mechanisms of alcohol-mediated organ and tissue damage: inflammation and immunity and alcohol and mitochondrial metabolism: at the crossroads of life and death session one: alcohol, cellular and organ Jan Hoek
Department of The University of Massachusetts Medical Center (GS and PM, Department of Medicine, Worcester, MA 01605-2324, USA
Alcohol Clin Exp Res 29:1735-43. 2005..by Kyle Happel 3) Decreased antigen presentation and anergy induced by alcohol in myeloid dendritic cells by Pranoti Mandrekar 4) Transcriptional regulation of TNF-alpha in human monocytes by chronic ethanol: role of the cellular redox .. - Acute alcohol consumption inhibits accessory cell function of monocytes and dendritic cellsGyongyi Szabo
Department of Medicine, University of Massachusetts Medical Center, Worcester, Massachusetts, USA
Alcohol Clin Exp Res 28:824-8. 2004..In this study, we investigated the effects of acute, moderate alcohol consumption on antigen presenting cell function of blood monocytes and monocyte-derived myeloid dendritic cells... - Acute alcohol inhibits the induction of nuclear regulatory factor kappa B activation through CD14/toll-like receptor 4, interleukin-1, and tumor necrosis factor receptors: a common mechanism independent of inhibitory kappa B alpha degradation?Pranoti Mandrekar
University of Massachusetts Medical School, Department of Medicine, Worcester 01605 2324, USA
Alcohol Clin Exp Res 26:1609-14. 2002..Here we investigated whether acute alcohol treatment of human monocytes also inhibits NF-kappaB when induced through activation of the interleukin (IL)-1 or tumor necrosis factor (TNF) receptors... - RSA 2004: combined basic research satellite symposium - session two: toll-like receptors and organ damagePranoti Mandrekar
Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605-2324, USA
Alcohol Clin Exp Res 29:1744-8. 2005.... - A recent perspective on alcohol, immunity, and host defenseGyongyi Szabo
Department of Medicine, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
Alcohol Clin Exp Res 33:220-32. 2009..Multiple line of clinical and experimental evidence demonstrates that both acute, moderate, and chronic, excessive alcohol use result in various abnormalities in the functions of the immune system... - FcgammaR cross-linking mediates NF-kappaB activation, reduced antigen presentation capacity, and decreased IL-12 production in monocytes without modulation of myeloid dendritic cell developmentYvonne Drechsler
Department of Medicine, University of Massachusetts Medical Center, Worcester, MA 01605, USA
J Leukoc Biol 72:657-67. 2002..These results suggest that signals mediated via FcgammaRI, -II, and -III have overlapping yet distinct effects on MO, which are likely to be involved in the fine-tuning of the immune responses to various stimuli... - Pattern recognition receptors: a contemporary view on liver diseasesGyongyi Szabo
Liver Center, Division of Gastroenterology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA
Hepatology 44:287-98. 2006..This review discusses the role of different PRRs in pathogen recognition in the liver, and focuses on the role of PRRs in hepatic inflammation, cholestasis, ischemia, repair and fibrosis. PRRs as novel therapeutic targets are evaluated... - Focus on: alcohol and the liverGyongyi Szabo
Division of Gastroenterology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts
Alcohol Res Health 33:87-96. 2010.... - Oxidative stress and inflammation: essential partners in alcoholic liver diseaseAditya Ambade
Department of Medicine, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 01605, USA
Int J Hepatol 2012:853175. 2012..Here we review major players of oxidative stress and inflammation and highlight signaling intermediates regulated by oxidative stress that provokes proinflammatory responses in alcoholic liver disease... - Cytokines and alcoholFulton T Crews
Bowles Center for Alcohol Studies, University of North Carolina, Chapel Hill, North Carolina 27599 7178, USA
Alcohol Clin Exp Res 30:720-30. 2006..Together these studies suggest that ethanol disruption of cytokines and inflammation contribute in multiple ways to a diversity of alcoholic pathologies...
Research Grants
- Heat shock proteins and alcohol induced liver injuryPranoti Mandrekar; Fiscal Year: 2006....
- Role of heat shock protein 90 in alcoholic liver diseasePranoti Mandrekar; Fiscal Year: 2010..Understanding these pathways will provide novel mechanisms and thus extend our horizons to identify potential new drug targets for alcoholic liver disease. ..