Neutrophils are best known for their role in host defense against microbes (1). However, many recent discoveries highlight the fact that neutrophils also act as key regulators of both acute and chronic sterile inflammatory conditions (2). Neutrophils can mediate their functions through different mechanisms, including generation of reactive oxygen species (ROS) and neutrophil extracellular traps (NETs), and the release of a broad range of mediators, including cytokines, alarmins, and proteases (1). A better knowledge of the mechanisms controlling these processes might thus help design new therapeutic strategies for the treatment of inflammatory diseases. This Research Topic brings together original and review articles that explore the role of neutrophils and neutrophil-derived products in various inflammatory diseases, and assess some molecular mechanisms through which these cells are activated in inflammatory conditions. It is known that lipopolysaccharide (LPS) from gram negative bacteria can "prime" neutrophil for ROS production in combination with other agonists. Liu et al. used pharmacological approaches to show that the prolyl cys/trans isomerase Pin1 plays an important role in LPS-induced priming of human neutrophils. These data suggest that Pin1 could be a therapeutic target in sepsis and other diseases involving ROS generation by neutrophils. Chiang et al. present an overview of the potential roles of neutrophils in psoriasis, a chronic inflammatory skin disease in which high numbers of neutrophils are observed in skin lesions. Their review focuses mostly on clinical observations, including evidence of neutrophil activation in skin lesions, with generation of ROS and formation of NETs. The authors also discuss the potential contribution of NETs in driving Th17 inflammation in psoriasis. Lastly, the potential role of NETs in infectious and inflammatory diseases has emerged as a major field of research (3, 4). Not surprisingly, several manuscripts of this special issue focus on the mechanisms of NET formation, and on the role of NETs in various inflammatory conditions. Barbu et al. describe a new method for the detection and quantification of histone H4 citrullination (H4cit3) during NET formation using imaging flow cytometry (IFC). Using this method, the authors quantify H4cit3 in human blood neutrophils stimulated with NET-triggering molecules. They suggest that their method can be particularly suitable for studies looking at NETs as potential biomarkers for diseases. The method is fast and requires only minimal handling of neutrophils.