**1. Introduction**

The polymorphonuclear neutrophils (PMNs), first reported by IIya IIych Mechnikov, better known as Élie Metchnikoff, are the most abundant leukocytes (60%) in the blood. These PMNs are considered as the first line of innate immune response against infectious agents [1]. Later on, Carl Friedrich Claus suggested the term of phagocytosis for the function of these cells. Studies aimed at the fully understanding of their properties and functions in controlling a variety of pathogens are still in progress. Research on neutrophils has focused on their

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phagocytic capacity and, more recently, on their role as neutrophil extracellular traps (NETs) forming cells, in innate and adaptive immunity.

When neutrophils fail to kill invading pathogens by the classical phagocytosis mechanism, PMNs can accomplish this function by neutrophil extracellular traps (NETs), a process reported as a novel form of cell death called NETosis, which is dependent of the generation of reactive oxygen species [2–5]. Neutrophils forming NETs have been demonstrated by activating neutrophils with phorbol myristate acetate (PMA), interleukin 8 (IL-8), lipopolysaccharide (LPS), or under contact of neutrophils with Gram-negative and Gram-positive bacteria.

NETosis induction has also been described for viral infections, and some of the signaling pathways involved have been analyzed, finding the involvement of pathogen-associated molecular patterns (PAMPs), TLR-4, TLR-7, and TLR-8. Rodríguez-Espinosa et al. have shown that NETs formation takes place in two separate metabolic steps: the first one involves chromatin decondensation, which is independent of external glucose and glycolysis, whereas the second, which involves the chromatin release, is a process that is dependent on external glucose and glycolysis [6].
