Some Lipids Act as Inflammatory Mediators

Following membrane perturbations, phospholipids in the membrane of several cell types (e.g., macrophages, monocytes, neutrophils, and mast cells) are degraded into arachidonic acid and lyso-platelet-activating factor (Figure 15-11). The latter is subsequently converted into platelet-activating factor (PAF), which causes platelet activation and has many inflammatory effects, including eosinophil chemotaxis and the activation and degranulation of neutrophils and eosinophils.

Metabolism of arachidonic acid by the cyclooxygenase pathway produces prostaglandins and thromboxanes. Different prostaglandins are produced by different cells: monocytes and macrophages produce large quantities of PGE2 and PGF2; neutrophils produce moderate amounts of PGE2; mast cells produce PGD2. Prostaglandins have diverse physiological effects, including increased vascular permeability, increased vascular dilation, and induction of neutrophil chemotaxis. The thromboxanes cause platelet aggregation and constriction of blood vessels.

Arachidonic acid is also metabolized by the lipoxygenase pathway to yield the four leukotrienes: LTB4, LTC4, LTD4, and LTE4. Three of these (LTC4, LTD4, and LTE4) together make up what was formerly called slow-reacting substance of anaphylaxis (SRS-A); these mediators induce smooth-muscle contraction. LTB4 is a potent chemoattractant of neutrophils. The leukotrienes are produced by a variety of cells, including monocytes, macrophages, and mast cells.

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Essentials of Human Physiology

Essentials of Human Physiology

This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.

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