**1. Introduction**

Neutrophils are the main effector cells of an acute inflammation. Their anti-inflammatory role is due to their specialised functions [1]. More than a decade ago, it was posited that, upon activation, neutrophils release extracellular structures composed of granular and nuclear constituents that neutralise bacteria. Since then, these fibrous networks have been called neutrophils extracellular traps (NETs) [2]. As this phenomenon was originally considered a particular form of cell death, different from necrosis or apoptosis, the process was labelled "NETosis" [3]. Recently, this concept has changed due to reports of two forms of NETosis: suicidal and vital [4]. The controversy continues as to whether a NETs release is a physiological host defence process or whether it is a consequence of cellular rupture [5]. It is important to be aware that robust effector functions may also lead to tissue damage [6]. The function of NETs is to offer a physical barrier that foils infectious spreading and raise the extracellular compartment of the concentration of antimicrobial substances [7]. Current research of NETs is expanding worldwide, and new research has uncovered new pathways in terms of understanding the mechanism for activating and releasing NETs. In the present review, we discuss the role of NETs in pathological responses, focusing specifically on eye diseases.
