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Bench Research:
Immune alterations induced by acute alcohol consumption: My laboratory is one of the few focusing on immunomodulation by moderate alcohol use in humans. In addition to understanding mechanisms for the increased susceptibility to infections after alcohol use, results from our investigations have relevance to decreased cardiovascular morbidity after moderate alcohol use as well as to accelerated liver disease in chronic hepatitis C virus infection. My laboratory studies changes in the interaction between accessory cells (monocytes and dendritic cells) and T lymphocytes after moderate alcohol use. The overall aim of our studies is to delineate the effect of alcohol on antigen presenting cell function and determine role of cytokine and co-stimulatory molecules leading to decreased antigen-specific T cell proliferation and impaired antimicrobial defense after alcohol use.
Intracellular signaling pathways in leukocytes mediating altered cytokine production after alcohol use. We are studying intracellular signaling mechanisms leading to decreased NF- B activation in monocytic and immune cells after acute alcohol treatment in relation to signals mediated by toll-like receptors. Recent interest is to define the NF-kB-mediated intracellular mechanisms that lead to the opposite effects of acute and chronic alcohol use on pro-inflammatory cytokine production.
Immune mechanisms leading to increased liver injury in HCV plus alcohol. The hypothesis is that impaired dendritic cell costimulatory activity is a pivotal defect of host response to hepatitis C infection and alcohol further reduces immunity by inhibiting maturation and functions of myeloid dendritic cells in HCV.
Immunopathogenesis of liver injury in obese mice: This is a developing project to investigate the hypothesis that leptin deficient, ob/ob mice have increased susceptibility to immune-mediated liver injury in a model of Concanavalin-A or LPS-induced hepatitis. We found that in contrast to lean mice, ob/ob mice have over-activation of the NF- B signaling pathway in the liver, a mechanisms likely to contribute to increased susceptibility to liver injury. Results from these experiments have direct clinical relevance to mechanisms of liver injury in non-alcoholic steatohepatitis in human.
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Journal of Hepatology (2024)
Urmila Jagtap, Anan Quan, Yuho Ono,Jonathan Lee, Kylie A. Shen, Sergei Manakov,Gyongyi Szabo, Imad Nasser,Frank J. Slack
Cancer Researchno. 6_Supplement (2024): 5689-5689
Gyongyi Szabo,Radhika Joshi,Veronika Brezani, Gabrielle M Mey,Sergi Guixé-Muntet,Marti Ortega-Ribera,Yuan Zhuang,Adam Zivny, Sebastian Werneburg,Jordi Gracia-Sancho
biorxiv(2024)
Natalia A. Osna,Irina Tikhanovich,Martí Ortega-Ribera,Sebastian Mueller, Chaowen Zheng,Johannes Mueller, Siyuan Li,Sadatsugu Sakane,Raquel Carvalho Gontijo Weber,Hyun Young Kim, Wonsoek Lee,Souradipta Ganguly,
Biomoleculesno. 4 (2024)
Hepatology (Baltimore, Md.) (2024)
The American journal of gastroenterologyno. 1 (2024): 107-115
Frontiers in Cell and Developmental Biology (2024): 1347395-1347395
HEPATOLOGY COMMUNICATIONSno. 12 (2023)
Prashanth Thevkar Nagesh,Yeonhee Cho,Yuan Zhuang,Mrigya Babuta,Radhika Joshi,Adriana Ramos, Jeeval Mehta,Christopher Copeland,Eleni Kanata, Zhenghui G. Jiang,Ioannis Vlachos,John M. Asara,
GASTROENTEROLOGYno. 6 (2023): S1265-S1265
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