Treatment in vitro with PPARα and PPARγ ligands drives M1-to-M2 polarization of macrophages from T. cruzi-infected mice.

摘要: Trypanosoma cruzi, the etiological agent of Chagas' disease, induces a persistent inflammatory response. Macrophages are first line cell phenotype involved in clearance infection. Upon parasite uptake, these cells increase mediators like NO, TNF-α, IL-1β and IL-6, leading to killing. Although desired, response perpetuation exacerbation may lead tissue damage. Peroxisome proliferator-activated receptors (PPARs) ligand-dependent nuclear transcription factors that, besides regulating lipid carbohydrate metabolism, have significant anti-inflammatory effect. This is mediated through interaction with their ligands. PPARγ, one PPAR isoforms, has been implicated macrophage polarization from M1, classically activated phenotype, M2, alternatively different models metabolic disorders In this study, we show for time PPARα also vitro macrophages isolated T. cruzi-infected mice. Polarization was evidenced by decrease expression NOS2 proinflammatory cytokines M2 markers Arginase I, Ym1, mannose receptor TGF-β. Besides, phagocytic activity significantly enhanced, increased load. We suggest that modulation both PPARs might be due, at least part, change profile macrophages. The potential use agonists as modulators overt during course disease deserves further investigation.