Intriguingly, these cells can now be consideredas having a paracrine action, attracting other neutrophils, as wellas dendritic cells and macrophages orchestrating the first steps tothe adaptive immune response activation.31 Lastly, we observed that neutrophils peak FPR1 expression4 h after infection, and this is a cell surface receptor for N-formylated peptides, typical of bacteria and mitochondrialproducts,32 giving strong evidence of theplasticity shown by neutrophil physiology in response to L. infantum infection and reinforcing the role ofmitochondrial components in inflammation process. The gene discussed is FPR1; the disease is infection.