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CEHS Graduate Student Receives PhRMA Fellowship

CEHS Toxicology Graduate Student Forrest Jessop Receives PhRMA Fellowship

Forrest Jessop was recently awarded the PhRMA Pre-doctoral Fellowship in Toxicology to assist dissertation research focused on chronic inflammatory diseases of the lung. This fellowship includes 2 years of stipend support ($20,000/year), the second year depending upon satisfactory progress in the first year, which begins January 1, 2014.  The award is highly competitive as the PhRMA Foundation only funds about 10 students per year, and only accepts one application per academic institution. The PhRMA foundation only funds students who have completed their graduate classwork, and can commit their time to dissertation research. This fellowship is awarded at a critical time in a graduate student’s education, and is intended to act as a stepping-stone for doctoral students in pharmacology and toxicology to become leaders in their fields and organizations. This award indicates the caliber not just of one CEHS graduate student, it also reflects the high level of training and support the CEHS Toxicology Graduate Studies program provides as a whole.

The title of Forrest's research proposal is: “Regulating Chronic NLRP3 Inflammasome Activity in the Lung through Autophagy.” Chronic inflammation is critical to the development of pulmonary fibrosis, a condition that decreases quality of life and is associated with a poor prognosis. There are no cures for pulmonary fibrosis. Many toxic agents can induce chronic inflammation through the NLRP3 inflammasome, a large protein complex that facilitates the release of pro-inflammatory mediators. Autophagy is an anti-inflammatory process activated, in part, to suppress inflammation by degrading inflammasome components. However, the mechanism by which NLRP3 inflammasome remains active in chronic inflammation, and is not suppressed by autophagy, is unknown.

The overall goal of this research fellowship is to define mechanisms that regulate chronic inflammatory disease in the lung, with the specific objective to delineate the cellular mechanism by which the NLRP3 inflammasome remains activated. This research aims to 1) elucidate the relationship between autophagy and NLRP3 inflammasome activity in models of chronic inflammatory lung disease, including silicosis and sarcoidosis, and 2) determine the effectiveness of therapeutically targeting autophagy to prevent chronic inflammation and reverse fibrosis.

Understanding mechanisms of chronic inflammation is needed to develop new therapies and prophylactic strategies. Due to the central importance of NLRP3 inflammasome and autophagy in chronic inflammatory disease, findings in this research fellowship will impact diseases beyond silicosis and sarcoidosis. Furthermore, the work from this proposal will provide the biological feasibility of targeting autophagy as an anti-inflammatory therapy for future clinical studies.