Research Assistant Professor
B.M. Sun Yat-Sen University, Guangzhou, China
M. MedSc. The University of Hong Kong, Hong Kong SAR, China
M.D. University of Duisburg-Essen, Faculty of Medicine Essen, Germany
I joined Dr. Billiar’s research group as a postdoctoral associate in the Department of Surgery in the University of Pittsburgh in Nov, 2010. I started a research project investigating the cell-specific roles of Toll-like receptor 4 (TLR4) in sepsis. Our work showed cell-type specific roles for TLR4 on myeloid cells and hepatocytes to regulate bacterial/LPS clearance and systemic inflammation during sepsis. My long term research interests involve assessing innate immune responses and the mechanisms that lead to immune dysregulation following sepsis injury.
Shedding of the tumor necrosis factor (TNF) receptor from the surface of hepatocytes during sepsis limits inflammation through cGMP signaling. Deng M, Loughran PA, Zhang L, Scott MJ, Billiar TR. Sci Signal. 2015 Jan 27;8(361):ra11. doi: 10.1126/scisignal.2005548. PMID: 25628461
Lipopolysaccharide stimulates p62-dependent autophagy-like aggregate clearance in hepatocytes. Chen C, Deng M, Sun Q, Loughran P, Billiar TR, Scott MJ. Biomed Res Int. 2014;2014:267350. doi: 10.1155/2014/267350. Epub 2014 Feb 10. PMID:24683544
Lipopolysaccharide clearance, bacterial clearance, and systemic inflammatory responses are regulated by cell type-specific functions of TLR4 during sepsis. Deng M, Scott MJ, Loughran P, Gibson G, Sodhi C, Watkins S, Hackam D, Billiar TR. J Immunol. 2013 May 15;190(10):5152-60. doi: 10.4049/jimmunol.1300496. Epub 2013 Apr 5. PMID:23562812