Ben Woolbright, PhD

Postdoctoral Fellow - Jaeschke Lab
B.S. in Biology, University of Kansas, 2006
Ph.D. in Toxicology, University of Kansas Medical Center, 2015

Born in Arkansas, but raised in Kansas, I graduated from the University of Kansas with a B.S. in Biology in 2006. I started my research career as a Ph.D. candidate in the Department of Pathology at Virginia Commonwealth University in the labs of Dr. Matthew Beckman, and subsequently Dr. Rakesh Kukreja, studying stem cell biology with the hope of enhancing the efficacy of stem cell transplantation therapy. I recently moved back to Kansas City to continue my education in the lab of Dr. Hartmut Jaeschke, pursuing a degree in Toxicology.

Research Interests

My interests scientifically are typically whatever I am doing in the moment. I enjoy Science more because of the process and the pursuit rather than for any one single interest. My hope is to be able to make a significant contribution to the field in some area that will directly impact quality of life for mankind.

Currently I am involved in a number of projects in the Jaeschke lab, however my main interest lies in the role of the neutrophil in cholestatic injury. Cholestasis is a part of multiple different pathologies including obstruction of the common bile duct, primary biliary cirrhosis, primary sclerosing cholangitis and intrahepatic familial cholestasis, and arises from different etiologies depending on which disease process is involved. While our lab has firmly established the neutrophil as a key mediator of cholestatic injury in extrahepatic cholestasis, we are currently trying to better define the role of the neutrophil in other models of cholestasis, as well as define new therapeutic targets for prevention of neutrophil mediated hepatic injury without complete immune suppression. To this end we employ multiple models of neutrophilic injury in the mouse, including surgical and nonsurgical models of cholestasis.


Jaeschke H, Woolbright BL. Current strategies to minimize hepatic ischemia-reperfusion injury by targeting reactive oxygen species. Transplant Rev (Orlando). 2012 Apr;26(2):103-14

Woolbright BL, Ramachandran A, McGill MR, Yan HM, Bajt ML, Sharpe MR, Lemasters JJ, Jaeschke H. Lysosomal instability and cathepsin B release during acetaminophen hepatotoxicity. Basic Clin Pharmacol Toxicol. 2012 Dec; 111(6):417-25.

Woolbright BL, Jaeschke H. Novel insight into mechanisms of cholestatic liver injury. World J Gastroenterol. 2012 Sep 28;18(36):4985-93.

Woolbright BL, Antoine DJ, Jenkins RE, Bajt ML, Park BK, Jaeschke H. Plasma biomarkers of liver injury and inflammation demonstrate a lack of apoptosis during obstructive cholestasis in mice. Toxicol Appl Pharmacol. 2013 Dec 15;273(3):524-31 doi: 10.1016/j.taap.2013.09.023

Woolbright BL, Li F, Xie Y, Farhood A, Fickert P, Trauner M, and Jaeschke H. Lithocholic acid feeding results in direct hepato-toxicity independent of neutrophil function in mice. Toxicol Lett. 2014 Apr 15. doi: 10.1016/j.toxlet.2014.04.001

Ni H, Woolbright BL, Copple C, Cui W, Luyendyke J, Jaeschke, H and Ding WX. Nrf2 Promotes the Development of Fibrosis and Tumorigenesis in Mice with Defective Hepatic Autophagy. J Hepatol. 2014 May 7. pii: S0168-8278(14)00306-7.

Woolbright BL, McGill MR, Staggs VS, Winefield RD, Gholami P, Olyaee M, Sharpe MR, Curry SC, Lee WM, Jaeschke H, and the ALF Study Group. Circulating Bile Acid Levels as Prognostic Biomarkers in Acetaminophen-induced Acute Liver Failure Patients. Toxicol Sci. Accepted.

Last modified: Mar 28, 2015



Ben Woolbright, PhD
Postdoctoral Fellow - Jaeschke Lab

4020 HLSIC; MS 1018
3901 Rainbow Blvd.
Kansas City, Kansas 66160

P: (913) 588-9184
F: (913) 588-7501