Session 3H: Effects of TLR4 and HMGB1 in the Liver
Session Number
Session 3H: 2nd Presentation
Advisor(s)
Jeannette Messer and Eugene Chang, University of Chicago
Location
Room A119
Start Date
28-4-2017 1:15 PM
End Date
28-4-2017 2:30 PM
Abstract
Toll Like Receptors are responsible for activating innate immunity in response to microbes. One such Toll Like Receptor is TLR4. TLR4 primarily senses lipopolysaccharide (LPS) from bacteria, but its response to LPS can be increased in the presence of the host stress response protein high mobility group box 1 (HMGB1). Bacterial LPS and HMGB1 have both been implicated in diet-induced fatty liver disease and type 2 diabetes, but the mechanisms whereby bacterial components and host stress responses contribute to these diseases are poorly understood. In this study we are investigating how HMGB1 and bacterial LPS from the intestine can influence disease in the liver.
Session 3H: Effects of TLR4 and HMGB1 in the Liver
Room A119
Toll Like Receptors are responsible for activating innate immunity in response to microbes. One such Toll Like Receptor is TLR4. TLR4 primarily senses lipopolysaccharide (LPS) from bacteria, but its response to LPS can be increased in the presence of the host stress response protein high mobility group box 1 (HMGB1). Bacterial LPS and HMGB1 have both been implicated in diet-induced fatty liver disease and type 2 diabetes, but the mechanisms whereby bacterial components and host stress responses contribute to these diseases are poorly understood. In this study we are investigating how HMGB1 and bacterial LPS from the intestine can influence disease in the liver.
Comments
Additional team members: Dr. Yun (Julia) Tao