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I’m a Ph.D. Candidate of Immunology and Parasitology at the University of Puerto Rico, Medical Science Campus and an NIH-RISE Fellow at the University of Puerto Rico, Rio Piedras Campus. My research project is focused on the anti-inflammatory role of Fasciola Hepatica GST protein in a murine DSS-induce colitis model. I am really interested in learning and working on science policy and technology commercialization. Now part of the NSF I-Corps family!
F. hepatica survives in the host by releasing excretory-secretory products (ESPs) that suppress the Th1 pro-inflammatory immune response and elicit a strong Th2/T-regulatory anti-inflammatory response. One of the proteins comprise in the ESPs is Glutathione S-Transferase (GST). Studies demonstrated that FhGST significantly suppresses the phosphorylation of numerous kinases and adapter molecules downstream TLR4 signaling cascade, including the NF-kB, which has been identified as a key regulator in the setting of inflammation caused by sepsis and ulcerative colitis (UC). UC is a chronic inflammatory disease characterized by extensive mucosal damage, significantly increased production of pro-inflammatory cytokines and retention of classically activated macrophages (M1-type). We hypothesize that FhGST could be an excellent therapeutic alternative to block the NF-kB activation, and favor a non-inflammatory phenotype during the setting of a dextran sulfate sodium (DSS) induced UC on mice.
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