Neutrophil extracellular traps generation and degradation in patients with granulomatosis with polyangiitis and systemic lupus erythematosus.

Neutrophils are one of the first cells to arrive at the site of infection, where they apply several strategies to kill pathogens: degranulation, respiratory burst, phagocytosis, and release of neutrophil extracellular traps (NETs). Recent discoveries try to connect NETs formation with autoimmune diseases, like systemic lupus erythematosus (SLE) or granulomatosis with polyangiitis (GPA) and place them among one of the factors responsible for disease pathogenesis. The aim of the study was to assess the NETotic capabilities of neutrophils obtained from freshly diagnosed autoimmune patients versus healthy controls.

Different procedures of diphenyleneiodonium chloride addition affect neutrophil extracellular trap formation.

A unique strategy, in which invading microorganisms are being caught in web-like structures composed mainly of DNA, involves a recently described phenomenon called NETosis. This process seems to be related to the production of reactive oxygen species (ROS). In our study, the influence of diphenyleneiodonium chloride (DPI), which diminishes ROS production, was assessed in the context of neutrophil extracellular trap (NET) release.

Neutrophil extracellular traps (Nets) impact upon autoimmune disorders.

Friend or foe? This is often asked question when it comes to neutrophil extracellular traps studies. There is no simple answer to that. At the time of their discovery they were considered to be protectors of our well-being.

Neutrophil extracellular traps in bacterial infections: strategies for escaping from killing.

Neutrophils are among the first responders to virulent factors. They kill microbes by phagocytosis, oxidative burst, and as neutrophil extracellular traps (NETs). NETs production leads to unique cell death depending on, inter alia, reactive oxygen species (ROS).