Neutrophils, a crucial component of the immune system, play a vital role in fighting bacterial infections through various mechanisms, including phagocytosis and degranulation. A more recent discovery is the formation of neutrophil extracellular traps (NETs), which involve the release of DNA and granular proteins into the extracellular environment to encapsulate and kill microorganisms. NETs are a form of programmed cell death distinct from apoptosis, necroptosis, and pyroptosis. The formation of NETs is triggered by various bacterial species and inflammatory mediators, leading to the release of DNA and histone proteins. NETs can be categorized into lytic and non-lytic forms, with the former involving cell lysis and the latter involving the expansion of the nucleus without lysis. Bacteria have evolved strategies to evade or resist NET-mediated antimicrobial effects. These strategies include inhibiting NET release, degrading NET components, and altering their surface properties. For example, bacteria can downregulate NET-stimulating phenotypes, inhibit NET-triggered molecules, suppress NET-mediated receptors on neutrophils, and interfere with NADPH signaling and ROS formation. Additionally, bacteria can degrade NET components such as DNA and proteins using nucleases and other enzymes. Some bacteria also exhibit resistance to the antimicrobial activity of NETs through capsule formation, biofilm formation, outer membrane vesicles, charge surface alteration, and secretion of antioxidant enzymes. Understanding the complex interplay between neutrophils, pathogens, and the immune system is crucial for developing therapeutic and diagnostic approaches to counteract bacterial evasion strategies and combat the role of NETs in inflammatory and autoimmune diseases. Maintaining a balanced and controlled NET release is essential for the proper functioning of the defense system and overall health.Neutrophils, a crucial component of the immune system, play a vital role in fighting bacterial infections through various mechanisms, including phagocytosis and degranulation. A more recent discovery is the formation of neutrophil extracellular traps (NETs), which involve the release of DNA and granular proteins into the extracellular environment to encapsulate and kill microorganisms. NETs are a form of programmed cell death distinct from apoptosis, necroptosis, and pyroptosis. The formation of NETs is triggered by various bacterial species and inflammatory mediators, leading to the release of DNA and histone proteins. NETs can be categorized into lytic and non-lytic forms, with the former involving cell lysis and the latter involving the expansion of the nucleus without lysis. Bacteria have evolved strategies to evade or resist NET-mediated antimicrobial effects. These strategies include inhibiting NET release, degrading NET components, and altering their surface properties. For example, bacteria can downregulate NET-stimulating phenotypes, inhibit NET-triggered molecules, suppress NET-mediated receptors on neutrophils, and interfere with NADPH signaling and ROS formation. Additionally, bacteria can degrade NET components such as DNA and proteins using nucleases and other enzymes. Some bacteria also exhibit resistance to the antimicrobial activity of NETs through capsule formation, biofilm formation, outer membrane vesicles, charge surface alteration, and secretion of antioxidant enzymes. Understanding the complex interplay between neutrophils, pathogens, and the immune system is crucial for developing therapeutic and diagnostic approaches to counteract bacterial evasion strategies and combat the role of NETs in inflammatory and autoimmune diseases. Maintaining a balanced and controlled NET release is essential for the proper functioning of the defense system and overall health.