Journal of Clinical Toxicology
Open Access
ISSN: 2161-0495
+44 1478 350008
ISSN: 2161-0495
+44 1478 350008
Isaac Downs
Scientific Tracks Abstracts: J Clinic Toxicol
U ncontrolled systemic activation of the immune system is an early initiating event that leads to development of acute fulminant liver failure (FLF) in mice after treatment with agonistic Fas mAb. In this study, we demonstrate that treatment of mice with N -acetylcysteine (NAC), an ROS scavenger and glutathione (GSH) precursor, almost completely abolished Fas mAb-induced FLF through suppression of V �± 14 i NKT cell activation, IFN-�³ signaling, apoptosis and nitrotyrosine formation in liver. In addition, enrichment of the liver with GSH due to V �± 14 i NKT cells deficiency, induced an anti-inflammatory response in the liver of J �± 18 â��/â�� mice that inhibited apoptosis, nitrotyrosine formation, IFN-�³ signaling and effectors functions. In summary, we propose a novel and previously unrecognized pro-inflammatory and pro-apoptotic role for endogenous ROS in stimulating T H 1 signaling in V �± 14 i NKT cells to promote the development of FLF. Therefore, our study provides critical new insights into how NAC, a ROS scavenger, regulates T H 1 signaling in intrahepatic V �± 14 i NKT cells to impact inflammatory and pathological responses
Isaac Downs has completed the requirements for his Ph. D from Louisiana State University Health Science Center and bachelor of cellular emphasis biology from Western Washington University. Isaac?s Ph. D thesis assessed the role of the innate immune T lymphocytes and reactive species for certain cases of acute liver failure. He has expertise in toxicology, immunology, pathology, pharmacology, physiology, and medicine