Grace Su, M.D.
Chief, Gastroenterology Section
Ann Arbor Veterans Administration Health Systems
Associate Professor,
Internal Medicine

gsu@umich.edu

Dr. Grace Su's research interests are in the area of hepatic innate immune responses to LPS and bacteria and its implications for liver injury and multi-system organ failure. In particular, Dr. Su laboratory has focused on the molecular mechanisms of Kupffer cell activation by lipopolysaccharide (LPS): role of LBP, CD14 and Toll like receptors. In addition, Dr. Su's laboratory is also examining the mechanisms of by which Kupffer cells kill bacteria. This is of particular importance in deciphering the pathway by which bacterial infections in patients with chronic liver failure can lead to multi-system organ failure. Other ongoing studies include examining the role of LBP and CD14 in several models of liver injury including alcoholic hepatitis and acute toxic liver injury.

Other collaborative studies involve determining the role of local LBP production on burn and lung injury as well as the role of protegrins on the treatment of burn injuries.

Study Projects

Molecular mechanisms Kupffer cell activation by LPS
Molecular mechanisms of bacterial killing by Kupffer cells
Role of LBP and CD14 in liver injury

Representative Publications

Su GL, Gong KQ, Fan MH, Kelley WM, Hsieh J, Sun JM, Hemmila MR, Arbabi S, Remick DG, Wang SC. Lipopolysaccharide binding protein modulates acetaminophen-induced liver injury in mice. Hepatology 41: 187-195, 2005.

Scott M, Liu S, Su GL, Vodovotz Y, Billiar TR. Hepatocytes enhance effects of lipopolysaccharide on liver nonparenchymal cells through direct cell- to-cell contact. Shock 23: 452-458, 2005.

Minter RM, Fan MH, Sun J, Niederbichler A., Ipaktchi K, Arbabi S, Hemmila MR, Remick DG, Wang SC, Su, GL. Altered Kupffer cell function in biliary obstruction. Surgery 138: 236-45, 2005.

Niederbichler AD, Hoesel LM, Westfall MV, Gao H, Ipaktchi KR, Sun L, Zetoune FS, Su GL, Arbabi S, Sarma VJ, Wang SC, Hemmila MR and Ward PA. An essential role for complement C5a in the pathogenesis of septic cardiac dysfunction. J Exp Med 203: 53-61, 2006.

Ipaktchi K, Mattar A, Niedlerbichler AD, Hoesel LM, Vollmannshauser S, Hemmila MR, Su GL, Remick DG, Wang SC, Arbabi S. Attenuating burn wound inflammatory signaling reduces systemic inflammation and acute lung injury. J. Immunol. 177:8065-71, 2006.

Hoesel LM, Niederbichler AD, Schafer J, Ipaktchi K, Gao H, Rittirsch D, Pianko MJ, Vogt PM, Vidya SJ, Su GL, Arbabi S, Westphall MV, Wang SC, Hemmila MR, Ward PA. C5a blockade improves burn induced cardiac dysfunction independent from endotoxin-mediated heart failure. J Immunol 178: 7902-7910, 2007.