Translational Science Initiative (TSI)

Lead PI: Carlos A. Sariol

Development of rhesus monkeys as a model of pre-diabetes
Dr. Sylvette Ayala, UPR-MSC

Like humans, rhesus monkeys develop spontaneous pre-diabetes followed by the overt condition during middle age. Rhesus monkeys comprise an accurate model for translational research to study the impact of pharmacological interventions on metabolic, molecular, and tissue pathological changes preceding IR/T2D. This project will take advantage of that to develop: 1) new models of pre-diabetes as powerful research tools available to the entire scientific community; and 2) new strategies for designing and testing novel interventions to prevent and treat metabolic diseases.


Induction of mucosal immunity in macaques by GVI adjuvants
Dr. Laura White, UNC

This project will test a new adjuvant able to induce mucosal immunity, which is critical for the HIV/AIDS immune response. The value of this adjuvant has been confirmed in mice models. By addressing the effects of this adjuvant in a nonhuman primate model, we will get closer to the translation into clinical trial.


Assessing the anti-inflammatory role of Fasciola hepatica fatty acid binding protein in a non-human primate septic shock model
Dr. Ana Espino, UPR-MSC

The present seeks to validate a molecule of parasitic origin termed Fh12 as a drug to prevent and treat septic shock. There are about 200,000 deaths caused by sepsis in the US each year. These deaths are primarily due to the persistence of a hyper activation of phagocytes that continuously secrete a storm of inflammatory cytokines, which result in hemorrhage, respiratory collapse and multi-organ failure. Although effective use of antibiotics has resulted in improved prognosis in many cases of sepsis, neutralization of inflammation is considered essential for preventing severe consequences of sepsis. A large number of bacterial products are responsible for the hyper activation of the phagocytes via TLRs-interaction. The development of antagonists that block either activation through TLRs or inhibit the storm of inflammatory molecules has become a priority in the search for novel anti-inflammatory drugs. We have strong preliminary data demonstrating that a single dose of 15μg of a 12kDa F. hepatica fatty acid binding protein (Fh12) is enough to prevent the inflammatory response induced by LPS-endotoxin in a mouse model of septic shock. The current project has two main focuses. First, to develop a non-human primate controlled septic shock model to study the change pattern of inflammatory cytokines during the early phase of septic shock, and second, to demonstrate that a single intravenous injection with Fh12 will prevent the inflammatory response induced by bacterial infection and will neutralize the inflammatory response after the onset of septic shock.