Phagocytosis
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Introduction
Phagocytosis, along with the release of enzymes by neutrophils and macrophages, is responsible for eliminating pathogens.
Phagocytosis involves three distinct steps:
- Recognition and attachment of the particle to be ingested. Mannose receptors bind to microbial wall sugars, while scavenger receptors bind to modified LDL particles and a variety of microbe proteins. Phagocytosis is greatly enhanced when microbes are opsonized by IgG, complement C3b, or mannose binding lectin.
- Engulfment of a particle occurs via extension of pseudopods around the particle and fusion of this vacuole with a lysosomal granule, resulting in progressive degranulation and killing of the organism.
Release of lysosomal granules before phagolysosomal closure, or frustrated phagocytosis, can result in endothelial injury and tissue damage. This is particularly important during chronic inflammation.
Following phagocytosis, neutrophils and macrophages kill and degrade infectious agents primarily using oxygen-dependent mechanisms.
Phagocytosis stimulates a burst of oxygen consumption, glycolysis, activity of the pentose-phosphate pathway, and production of reactive oxygen species (ROS, aka ROIs).
Production of ROS is due to NADPH oxidation. Hydrogen peroxide is combined with Cl- to create HOCl, which effectively destroys microbes by halogenation. Oxygen-independent mechanisms include lysozyme, lactoferrin, defensins, and other enzymes. After killing, acid hydrolases degrade microbes as the pH dips to between 4 and 5.
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