Reben Raeman, MS, PhD
Assistant Professor of Pathology

Dr. Raeman
Dr. Raeman is a member of the Division of Experimental Pathology.

Office Location:
University of Pittsburgh
Department of Pathology
200 Lothrop St, Room S-408
Pittsburgh, PA 15261

Contact Information:
Office Telephone: 412-648-2021
Email: reben.raeman@pitt.edu

Education

  • BS - ANGRAU, Hyderabad, India, 2001
  • MS Clemson University, Clemson, SC, 2006
  • PhD - University of Georgia, Athens, GA, 2011
  • Postdoctoral fellowship - Emory University, Atlanta, GA, 2012 - 2013
  • Postdoctoral fellowship - Emory University, Atlanta, GA, 2013 - 2016

Research Interests

The primary focus of our lab is to elucidate host and environmental factors driving hepatic inflammation and fibrosis in non-alcoholic steatohepatitis (NASH). NASH is an advanced and progressive form of non-alcoholic fatty liver disease affecting ~16.5 million people in the US. An estimated one in six patients with NASH progress to cirrhosis, and NASH-related cirrhosis is now the 2nd leading cause of liver transplantation in the US. Consequently, there is an urgent need to devise novel therapeutic interventions to halt progression of NASH, as no therapies currently exist. We have recently established that gut microbial antigens are among the primary drivers of hepatic inflammation and fibrosis in NASH. Our findings also underscore the importance of diet-induced gut dysbiosis, mucosal inflammation, and subsequent disruption of the intestinal epithelial barrier in NASH. The mouse model of compromised intestinal epithelial barrier we used for these studies turned out to be an excellent dietary model of NASH. When fed a Western diet, these mice not only develop key features of MetS, but also develop hepatic inflammation and fibrosis. Using this novel preclinical model, we are performing further studies to gain mechanistic insights into the etiology of NASH progression. Our overarching goal is to dissect the complex interplay between intestinal epithelial barrier, gut microbial dysbiosis, and immune dysregulation in NASH. The ultimate goal of our research is to devise preventative and therapeutic modalities for the clinic.

We are currently exploring three major questions:

  1. How does gut microbiota modulate intestinal epithelial barrier permeability and mucosal immunity in NASH?
  2. Role of adaptive immune responses, specifically T cells, in regulating hepatic inflammation in NASH.
  3. How do diet induced changes in bile acid composition impact colonic epithelial barrier?

Selected Publications

  • Chopyk, D.M., P. Kumar, Reben Raeman, Y. Liu, T. Smith, F.A. Anania. Dysregulation of junctional adhesion molecule-A contributes to ethanol-induced barrier disruption in intestinal epithelial cell monolayers. Physiol Rep. 2017 Dec 5(23).
  • Reben Raeman, F.A. Anania. Therapy for steatohepatitis: Do macrophages hold the clue? Hepatology. 2017 Nov 1. PMID: 29091293.
  • Tedesco, D., M. Thapa, S. Gumber, E.J. Elrod, K. Rahman, C.C Ibegbu, J.F. Magliocca, A.B. Adams, F. Anania, A. Grakoui. CD4+ Foxp3+ T cells promote aberrant IgG production and maintain CD8+ T cell suppression during chronic liver disease. Hepatology. 2016 Oct 24. PMID: 27774611
  • Rahman, K.*, C. Desai, S.S. Iyer, N. Thorn, P. Kumar, L. Yunshan, T. Smith, A.S. Neish, H. Li, S. Tan, P. Wu, X. Liu, Y. Yu, A.B. Farris, A. Nusrat, C.A. Parkos, F.A. Anania. Loss of Junctional Adhesion Molecule A Promotes Severe Steatohepatitis in Mice on a Diet High in Saturated Fat, Fructose, and Cholesterol. Gastroenterology, 2016. Oct; 151(4):733-746. *, co-corresponding author.
  • Rahman, K.*, Y. Liu, P. Kumar, T. Smith, N.E. Thorn, A.B. Farris, F.A. Anania. C/EBP homologous protein modulates liraglutide-mediated attenuation of non-alcoholic steatohepatitis. Lab Invest, 2016. Aug; 96(8): 895-908. *, corresponding author.
  • Go Y.M., R.L. Sutliff, J.D. Chandler, K. Rahman, B.Y. Kang, F.A. Anania, M. Orr, L. Hao, B.A. Fowler, D.P. Jones. Low-Dose Cadmium Causes Metabolic and Genetic Dysregulation Associated With Fatty Liver Disease in Mice. Toxicol. Sci., 2015, 147(2): 524-34.
  • Tabatabavakili, S., R. Kailar, K. Rahman, B. Nezami, S. Mwangi, F. Anania, S. Srinivasan. Glial Cell Line-Derived Neurotrophic Factor induced Mice Liver Defatting: A Novel Strategy to Enable Transplantation of Steatotic Livers. Liver Transplantation, 2016, 22(4): 459-67.
  • Kumar P., T. Smith, K. Rahman, J.E. Mells, N.E. Thorn, N.K. Saxena, F.A. Anania. Adiponectin modulates focal adhesion disassembly in activated hepatic stellate cells: implication for reversing hepatic fibrosis. FASEB, 2014, J. 28(12): 5172-83.
  • Kumar P., S. Tekla, K. Rahman, N. Thorn, F.A. Anania. Adiponectin agonist ADP355 attenuates CCl4-induced liver fibrosis in mice. PLoS, 2014, One. 13; 19(10).
  • Rahman, K., S.S. Iyer. Costimulatory molecules as vaccine adjuvants: to 4-1BB or not to 4-1BB? Cell Mol Immunol. 2014, 1-2.
  • Rahman, K., M. Sasaki, A. Nusrat and J.M.A. Klapproth. Crohn's disease-associated Escherichia coli survive in macrophages by suppressing NF?B signaling. Inflamm. Bowel Dis., 2014, 20(8): 1419-1425.