Interference of the Inflammasome Via Interferon-β
It is well established that macrophages, a classification of white blood cells, are the body’s first line of defense against stressors such as bacterial and viral infections. The inflammatory response is adaptive and is the body’s way of fighting anything that would be considered foreign, and therefore potentially dangerous to the human body. This project looks at metabolic diseases, such as obesity and type 2 diabetes mellitus (T2DM), and the pro-inflammatory phenotype. The pro-inflammatory phenotype is a physical manifestation of the molecular changes that take place due to the high fat environment associated with metabolic diseases. This inflammatory response has been associated with not only metabolic disorder, but also Alzheimer’s Disease, atherosclerosis, autoinflammatory/ autoimmune diseases, gout, inhibited tissue repair and creation of tumors. This project aims to assess a specific protein called PPAR-γ that, when absent, has been shown to decrease this pro-inflammatory response. If the mechanism behind how this protein works to decrease the inflammatory response can be established, it could be used clinically to treat many of the inflammatory conditions. It is hypothesized that that in the absence of PPAR-γ a signaling molecule called IFN-β is increased, leading to the anti-inflammatory response. It is unknown how IFN-β and PPAR-γ are linked mechanistically. Through this research, we hope to establish the link between these two molecules. If this novel mechanism can be established, it can be used therapeutically to decrease the pro-inflammatory response.
Anne R Crecelius
Primary Advisor's Department
Health and Sport Science
Stander Symposium poster
"Interference of the Inflammasome Via Interferon-β" (2018). Stander Symposium Posters. 1152.