Neutrophils are specialized white blood cells primarily responsible for phagocytosis, the process of engulfing and destroying foreign particles and cellular debris.

Neutrophils can perform both opsonization-dependent phagocytosis, which involves the recognition of opsonized particles via surface receptors, and opsonization-independent phagocytosis, where they directly recognize and engulf non-opsonized particles.

Neutrophils express various surface receptors, including Fc receptors for recognizing antibodies bound to pathogens and complement receptors for recognizing complement proteins deposited on pathogens, enabling opsonization-dependent phagocytosis.

NADPH oxidase is an enzyme complex present in neutrophils that generates reactive oxygen species (ROS) during phagocytosis. ROS play a crucial role in killing and destroying engulfed pathogens.

Neutrophils release various antimicrobial peptides during phagocytosis, including defensins, cathelicidins, and S100 proteins. These peptides have broad-spectrum antimicrobial activity against bacteria, fungi, and viruses.

Neutrophil extracellular traps (NETs) are structures formed by neutrophils during phagocytosis. NETs consist of DNA, histones, and antimicrobial proteins. They immobilize and kill pathogens, recruit other immune cells to the site of infection, and contribute to the overall host defense.

Interleukin-8 (IL-8) is a potent chemotactic cytokine that plays a crucial role in neutrophil recruitment to the site of infection. It is produced by various cell types, including macrophages, endothelial cells, and epithelial cells, in response to infection or tissue damage.

Neutrophils have a relatively short lifespan in the bloodstream, typically ranging from 6 to 12 hours. After this period, they either migrate into tissues or undergo apoptosis.

Neutrophil-mediated tissue damage occurs when neutrophils release excessive amounts of reactive oxygen species (ROS), antimicrobial peptides, and proteolytic enzymes, leading to tissue destruction. This can contribute to the pathogenesis of various inflammatory diseases.

Neutrophils employ a combination of mechanisms to kill ingested pathogens. Phagocytosis involves engulfing the pathogen, degranulation releases antimicrobial peptides and enzymes into the phagosome, and the respiratory burst generates reactive oxygen species (ROS) that contribute to pathogen killing.

Chronic granulomatous disease (CGD), leukocyte adhesion deficiency (LAD), and severe congenital neutropenia (SCN) are genetic disorders that result in impaired neutrophil function. CGD affects the production of reactive oxygen species (ROS), LAD affects neutrophil adhesion and migration, and SCN leads to a deficiency in neutrophil production.

Neutrophils play a crucial role in the innate immune response by recognizing foreign pathogens through pattern recognition receptors (PRRs), activating the complement system via the release of complement proteins, and releasing inflammatory mediators such as cytokines and chemokines to recruit other immune cells to the site of infection.

Neutrophil activation can be triggered by various signaling pathways, including Toll-like receptor (TLR) signaling, Fc receptor (FcR) signaling, and complement receptor (CR) signaling. These pathways lead to the production of reactive oxygen species (ROS), antimicrobial peptides, and the release of inflammatory mediators.

Reactive oxygen species (ROS) play a crucial role in the killing of ingested pathogens by neutrophils. ROS are generated during the respiratory burst and have potent antimicrobial activity against a wide range of microorganisms.

NADPH oxidase is the enzyme responsible for the production of reactive oxygen species (ROS) in neutrophils. It is activated during phagocytosis and generates superoxide anions, which are subsequently converted into other ROS, including hydrogen peroxide and hypochlorous acid.