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Phagocytosis is the ingestion by individual cells of invading foreign particles, such as bacteria. It is a critical protective mechanism of the immune system. Many microorganisms release substances that attract phagocytic cells. Phagocytosis may be enhanced by a variety of factors that make the foreign particle an easier target. These factors, collectively referred to as opsonins (the Greek word meaning “prepare food for”), consist of antibodies and various serum components of complement (see Chapter 4). After ingestion, the foreign particle is entrapped in a phagocytic vacuole (phagosome), which fuses with lysosomes, forming the phagolysosome. The latter releases its powerful enzymes, which digest the particle.

Phagocytes can also damage invading pathogens through the generation of toxic products in a process known as the respiratory burst. Production of these toxic metabolites is induced during phagocytosis of pathogens such as bacteria and catalyzed by a set of interrelated enzyme pathways. The most important of these are nitric oxide (inducible nitric oxidase synthase), hydrogen peroxide and superoxide anion (phagocyte NADPH oxidase), and hypochlorous acid (myeloperoxidase), each of which is toxic to bacteria. These microbicidal products can also damage host cells. Fortunately, a series of protective enzymes produced by phagocytes controls the action of these products so that their microbicidal activity is primarily limited to the phagolysosome (i.e., fused phagosomes and lysosomes; see Figure 3.8), thereby focusing their toxicity on ingested pathogens. These protective enzymes include catalase, which degrades hydrogen peroxide, and superoxide dismutase, which converts the superoxide anion into hydrogen peroxide and oxygen. The absence of, or an abnormality in, any one of the respiratory burst components from phagocytic cells results in a form of immunodeficiency that predisposes individuals to repeated infections (see Chapter 16).

Figure 3.8. Endocytosis and phagocytosis by phagocytes.