BIOE-3020 Lecture Notes - Lecture 15: Neutrophil, Phenotype, Fibrinogen
25 Aug 2016
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Document Summary
A small vascular injury initiates the complement alternative pathway. The disturbed endothelial cells produce enzymes, which cleave extracellular protein c3. C3b is a sticky protein that adsorbs at the injury site and catalyzes cleavage of c5 into c5a and. C5a is a soluble ligand and chemotactic factor that recruits neutrophils and monocytes to the site of vascular injury (travel along the vascular wall) where they bind to c3b. Chemotactic factors include kallikrein, fibrinopeptides released from fibrinogen, and fibrin degradation products. Neutrophils arrive first, as they are present in the blood in about 10 times greater concentration than monocytes. Monocytes become macrophages as a result of a phenotypical transition. The wound healing (chronic inflammation) process leads to the formation of oxidized ldls. Being a lipid, ldl is extremely susceptible to oxidation. Nadph (nicotinamide adenine dinucleotide phosphate) oxidase, present in activated neutrophils and macrophages, oxidizes. Ldl to oxidized ldl (ox-ldl) at the injury site.
