Public university in San Luis, Argentina
My career has been highlighted by a productive research on oxidative stress and inflammation induced by macrophages at sites of tissue irritation caused by metabolic and environmental stressors. I was involved in improving methods to see and prevent the oxidative damage to macromolecules and found that the nitrones spin trap DMPO can be used as a discovery tool, and also as a therapeutic to ameliorate inflammation. I strongly believe that hypoxic inflammation may play a role in controlling the biology of the tumor and “obese” fat tissue inflammation. Interestingly in both monocyte infiltration and macrophage M1/M2 switch can be controlled by the hypoxic inflammation installed in these microenvironments. Data gathered from our combined efforts to understand the role of macrophage biology at sites of hypoxic inflammation and metabolic switch at stressed microenvironments will provide mechanisms and targets to prevent “obese” fat tissue inflammation and tumor invasiveness/resistance. On the other hand our projects are focused in the mechanism linking inflammation of the obese lung and insulin resistance, with emphasis in neutrophils and oxidations promoted by activation of myeloperoxidase (MPO). Our models in vitro and in vivo of Western diet-induced obesity are allowing to test whether natural and synthetic products to inhibit MPO, reduce NF-kB activation and activate Nrf-2. Nrf-2 and PPAR-δ agonists can prove to be effective to increase adipogenesis and to reduce macrophage switch towards an inflammatory phenotype.