Phagocytosis and neutrophil extracellular traps

Abstract

Neutrophils are recruited rapidly to sites of infection in response to host- and/or microbe-derived proinflammatory molecules. At such sites, neutrophils phagocytose microbes and are activated to produce superoxide and other reactive oxygen species (ROS). In addition, neutrophils contain stores of antimicrobial peptides and enzymes that work in concert with ROS to kill ingested microbes. Neutrophils can also release chromosomal DNA bound with antimicrobial peptides and enzymes to form web-like structures known as extracellular traps. Neutrophil extracellular traps (NETs) have been reported to ensnare and kill microbes and are commonly considered to be an important component of innate host defense. Notably, the formation of NETs is most often reported as a cytolytic process. Whereas intraphagosomal killing of microbes sequesters cytotoxic antimicrobial molecules that would otherwise damage host tissues, the formation of NETs and associated extracellular release of these molecules can contribute to host tissue destruction and disease. Here we compare and contrast phagocytosis and NETs in host defense, with emphasis on recent studies of NETs that ultimately underscore the importance of phagocytosis as the primary means by which neutrophils eliminate microbes.

Keywords: NETs; Neutrophil; neutrophil extracellular trap; phagocytosis.