A key function of neutrophils is to attack and kill bacteria at sites of infection. Bacteria are phagocytosed and fusion of phagocytic vacuoles with neutrophil granules exposes the bacteria to a collection of antimicrobial reagents, including lytic enzymes, cationic peptides that disrupt bacterial membranes and reactive oxygen species. Neutrophils can also kill bacteria extracellularly, and a new study from Volker Brinkmann and colleagues reveals that this is achieved by concentrating antimicrobial reagents in a fibrous network released by the neutrophil.

Neutrophils were stimulated with interleukin-8, phorbol myristate acetate or lipopolysaccharide. When the activated neutrophils were gently washed and fixed, and examined by high-resolution scanning electron microscopy, Brinkmann and colleagues observed fibrous extracellular structures outside the cells. These were termed neutrophil extracellular traps or NETs. The NETs were composed of DNA, histones and granule enzymes, such as neutrophil elastase, and were released from the cells as early as 10 minutes after activation. NETS were able to trap both Gram-positive and Gram-negative bacteria. Blocking the function of neutrophil proteases showed that they were required for the deactivation of bacterial virulence factors. NETs were also observed in vivo in samples taken from shigellosis infection of rabbits and appendicitis in humans.

Extracellular killing of bacteria carries the risk of damaging the host cells by exposing them to the neutrophil's antimicrobial toolkit. The authors suggest that NETs amplify the activity of antimicrobial components by concentrating them in the fibrous network, which should also reduce exposure of host tissue to these components. It remains to be determined whether NETs are formed by an active process or are an early stage in neutrophil cell death.