Similarly, PPAR-γ levels were elevated by ~ 1.48-fold after infection relative to the uninfected control, whereas ApoA1 priming followed by Ld infection led to a ~ 1.64-fold decrease in PPAR-γ expression compared to the Ld-infected group (Fig. 5), suggesting the role of ApoA1 in blocking M2 polarization during Leishmania infection. This evidence concerns the gene APOA1 and infection.