Editing Inflammation (section)

=== Phagocytosis ===
{{Main|Phagocyte}}
Extravasated neutrophils in the cellular phase come into contact with microbes at the inflamed tissue. [[Phagocyte]]s express cell-surface endocytic [[pattern recognition receptors]] (PRRs) that have affinity and efficacy against non-specific [[microbe-associated molecular patterns]] (PAMPs). Most PAMPs that bind to endocytic PRRs and initiate [[phagocytosis]] are cell wall components, including complex carbohydrates such as [[mannans]] and β-[[glucans]], [[lipopolysaccharides]] (LPS), [[peptidoglycans]], and surface proteins. Endocytic PRRs on phagocytes reflect these molecular patterns, with [[C-type lectin]] receptors binding to mannans and β-glucans, and [[scavenger receptor (immunology)|scavenger receptor]]s binding to LPS.

Upon endocytic PRR binding, [[actin]]-[[myosin]] [[cytoskeletal]] rearrangement adjacent to the plasma membrane occurs in a way that [[endocytosis|endocytoses]] the plasma membrane containing the PRR-PAMP complex, and the microbe. [[Phosphatidylinositol]] and [[Vps34]]-[[PIK3R4|Vps15]]-[[BECN1|Beclin1]] signalling pathways have been implicated to traffic the endocytosed phagosome to intracellular [[lysosomes]], where fusion of the phagosome and the lysosome produces a phagolysosome. The [[reactive oxygen species]], [[superoxides]] and [[hypochlorite]] bleach within the phagolysosomes then kill microbes inside the phagocyte.

Phagocytic efficacy can be enhanced by [[opsonization]]. Plasma derived complement [[C3b]] and antibodies that exude into the inflamed tissue during the vascular phase bind to and coat the microbial antigens. As well as endocytic PRRs, phagocytes also express [[opsonin]] receptors [[Fc receptor]] and [[complement receptor 1]] (CR1), which bind to antibodies and C3b, respectively. The co-stimulation of endocytic PRR and opsonin receptor increases the efficacy of the phagocytic process, enhancing the [[lysosomal]] elimination of the infective agent.