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Pranoti Mandrekar, Ph.D.

 

Other Affiliation(s):

Director, Translational Science Program
Director, NIH Summer Research Program

Graduate School of Biomedical Sciences

 

STRESS RESPONSES AND PROTEOSTASIS REGULATORS IN LIVER INFLAMMATION ANND FIBROSIS

Research in my laboratory focuses on understanding the signaling mechanisms involved in innate immune cell activation during liver injury and cancer. The physiological function of the liver is elimination of pathogens and antigens from the blood for which mounting of an immune response is required. To avoid unnecessary activation of the immune system, the liver develops a local immune response followed by induction of peripheral tolerance towards the antigen. When stressful agents such as pathogens or environmental insults challenge the liver for extended periods of time and their elimination is not possible, inflammation and injury follows. The onset of inflammation in the liver is followed by fibrosis, cirrhosis and liver cancer. Thus, studying the mechanisms involved in liver inflammation will provide major insights into pathogenesis of liver disease and progression.

Using various in vivo and in vitro models, we are studying the role of innate immune signaling pathways, their crosstalk with oxidative stress mechanisms leading to pro-inflammatory cytokine production. We are also focusing on investigating the role of chemokine responses and their effect on recruitment of bone-marrow derived cells and immune cells in the liver during development and progression of liver disease. Recent studies initiated in our lab focus on the impact of alcohol drinking on breast and liver cancer. Th main areas of focus are:

1) Proteostasis mechanisms in fatty liver disease, inflammation and fibrosis

Characterization of an interplay of immune and oxidative stress related mechanisms involved in mediating the effects of acute and chronic alcohol consumption, and epigenetic pathways altered in chronic liver diseases using alcoholic and non-alcoholic liver disease models are being studied. We identified a pathogenic role for stress mediated transcription factor HSF1 and its target gene, hsp90 and hsp70 in innate immune cells resulting in regulation of inflammatory responses. Using molecular and targeted translational approaches we are currently evaluating hsp90 and hsp70 as a therapeutic targets in manipulation of macrophage function in host defense and liver diseases such as alcoholic liver disease and fibrosis.

2) Gut-liver-brain Axis in Liver Diseases

The impact of

3) Adipose-Liver Crosstalk

 

4) Chemokines and importance of immune liver cell types in liver injury

The dynamic role of immune cells and bone marrow derived hematopoietic cells and their cross talk with other liver cell types in promoting liver diseases is being investigated. Liver macrophages, dendritic cells, NK and NKT cells play an important function in development and progression of liver disease. We propose to unravel the role of chemokinesin recruitment of immune cells in the liver and modulate chronic liver injury. Specifically, studies from our laboratory have identified a significant role for a CC-chemokine, monocyte chemoattractant protein -1 (MCP-1) in induction of fatty liver disease. We hypothesize that CCL2 is an important link between innate immune mechanisms and steatosis or fatty liver. Other chemokines and chemokine receptors are also being explored to determine the role of MCP-1 in mediating inflammatory processes leading to alcoholic liver injury.

 

 

 


One or more keywords matched the following items that are connected to Mandrekar, Pranoti

Item TypeName
Academic Article Regulation of human monocyte functions by acute ethanol treatment: decreased tumor necrosis factor-alpha, interleukin-1 beta and elevated interleukin-10, and transforming growth factor-beta production.
Academic Article Alcohol-induced regulation of nuclear regulatory factor-kappa beta in human monocytes.
Academic Article Regulation of monocyte IL-12 production: augmentation by lymphocyte contact and acute ethanol treatment, inhibition by elevated intracellular cAMP.
Academic Article Acute alcohol consumption attenuates interleukin-8 (IL-8) and monocyte chemoattractant peptide-1 (MCP-1) induction in response to ex vivo stimulation.
Academic Article Inhibition of lipopolysaccharide-mediated NFkappaB activation by ethanol in human monocytes.
Academic Article Human monocyte IL-10 production is increased by acute ethanol treatment.
Academic Article Acute ethanol treatment augments interleukin-12 production in activated human monocytes.
Academic Article Regulation of monocyte interleukin-12 production by acute alcohol: a role for inhibition by interleukin-10.
Academic Article Reduced alloreactive T-cell activation after alcohol intake is due to impaired monocyte accessory cell function and correlates with elevated IL-10, IL-13, and decreased IFNgamma levels.
Academic Article FcgammaR cross-linking mediates NF-kappaB activation, reduced antigen presentation capacity, and decreased IL-12 production in monocytes without modulation of myeloid dendritic cell development.
Academic Article Inhibition of NF-kappa B binding correlates with increased nuclear glucocorticoid receptor levels in acute alcohol-treated human monocytes.
Academic Article Acute alcohol consumption inhibits accessory cell function of monocytes and dendritic cells.
Academic Article Acute ethanol treatment modulates Toll-like receptor-4 association with lipid rafts.
Academic Article Moderate alcohol intake in humans attenuates monocyte inflammatory responses: inhibition of nuclear regulatory factor kappa B and induction of interleukin 10.
Academic Article TLR2- and TLR4-mediated signals determine attenuation or augmentation of inflammation by acute alcohol in monocytes.
Academic Article Viral and host factors induce macrophage activation and loss of toll-like receptor tolerance in chronic HCV infection.
Academic Article Interferon alpha and alcohol augment nuclear regulatory factor-kappaB activation in HepG2 cells, and interferon alpha increases pro-inflammatory cytokine production.
Academic Article Alcohol exposure regulates heat shock transcription factor binding and heat shock proteins 70 and 90 in monocytes and macrophages: implication for TNF-alpha regulation.
Academic Article Tacrolimus and cyclosporine A inhibit allostimulatory capacity and cytokine production of human myeloid dendritic cells.
Academic Article Ethanol-mediated regulation of transcription factors in immunocompetent cells.
Academic Article Hepatitis C virus core and nonstructural protein 3 proteins induce pro- and anti-inflammatory cytokines and inhibit dendritic cell differentiation.
Academic Article Inhibition of superantigen-induced T cell proliferation and monocyte IL-1 beta, TNF-alpha, and IL-6 production by acute ethanol treatment.
Academic Article Cytokines and alcohol.
Academic Article Heme oxygenase-1 mediates the anti-inflammatory effects of acute alcohol on IL-10 induction involving p38 MAPK activation in monocytes.
Academic Article Hepatitis C virus (HCV) core protein-induced, monocyte-mediated mechanisms of reduced IFN-alpha and plasmacytoid dendritic cell loss in chronic HCV infection.
Academic Article Acute alcohol exposure exerts anti-inflammatory effects by inhibiting IkappaB kinase activity and p65 phosphorylation in human monocytes.
Academic Article Acute alcohol activates STAT3, AP-1, and Sp-1 transcription factors via the family of Src kinases to promote IL-10 production in human monocytes.
Academic Article Effect of ethanol on inflammatory responses. Implications for pancreatitis.
Academic Article Human monocytes, macrophages, and dendritic cells: alcohol treatment methods.
Academic Article Acute alcohol intake induces SOCS1 and SOCS3 and inhibits cytokine-induced STAT1 and STAT3 signaling in human monocytes.
Academic Article The opposite effects of acute and chronic alcohol on lipopolysaccharide-induced inflammation are linked to IRAK-M in human monocytes.
Academic Article An essential role for monocyte chemoattractant protein-1 in alcoholic liver injury: regulation of proinflammatory cytokines and hepatic steatosis in mice.
Academic Article Acute ethanol consumption synergizes with trauma to increase monocyte tumor necrosis factor alpha production late postinjury.
Concept Monocytes
Academic Article Moderate alcohol induces stress proteins HSF1 and hsp70 and inhibits proinflammatory cytokines resulting in endotoxin tolerance.

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  • Monocytes