f Phagocytosis ingestion of microbes or other particles such as cellular debris

F phagocytosis ingestion of microbes or other

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f. Phagocytosis: ingestion of microbes or other particles such as cellular debris. Occurs in 5 phases: 1. Chemotaxis: chemically stimulated movement of phagocytes to a cite of damage
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2. Adherence: attachment of phagocyte to the microbe or other foreign material. The binding of complement proteins to the invading pathogen enhance adherence. 3. Ingestion: the plasma membrane of the phagocyte extends projections, called pseudopods, which engulf the microbe. 4. Digestion: the phagosome enters the cytoplasm and merges with lysosomes to form a single, larger structure called a phagolysosome. The lysososome contributes lysozyme, which breaks down microbial cell walls, and other digestive enzymes that degrade carbs, proteins, lipids and nucleic acids. 5. Killing: the chemical onslaught provided by the lysozyme, digestive enzymes, and oxidants within the phagolysosome quickly kills many types of microbes. V. Inflammation: is a nonspecific, defensive response of the body to tissue damage. Among the conditions that may produce inflammation are pathogens, abrasions, chemical irritations, distortion or disturbances of cells, and extreme temperatures. The inflammatory response has 3 basic stages 1) vasodilation and increased permeability of blood vessels 2) emigration of phagocytes from blood into interstitial fluid 3) tissue repair. a. Redness, pain, heat and swelling: signs and symptoms of inflammation b. Loss of function: inflammation can also cause loss of function in the injured area depending on the site and extent of the injury. VI. Vasodilation and increased blood vessel permeability: allows more blood flow to the damaged area, and increased permeability permits defensive proteins such as antibodies and clotting factors to enter the injured area from the blood. VII. Histamine: causes vasodilation and increased permeability of blood vessels. VIII. Kinins: induce vasodilation and increased permeability and serve as chemotactic agents for phagocytes. IX. Prostaglandins: are released by damaged cells and intensify the effects of histamines and kinins. X. Leukotrienes: cause increased permeability. They also function in adherence of phagocytes to pathogens and as chemotactic agents that attract phagocytes. XI. Complement: different components of the complement system stimulate histamine release, attract neutrophils by chemotaxis, and promote phagocytosis; some components can also destroy bacteria. XII. Emigration: phagocytes appear on the scene within an hour. As large amounts of blood accumulate, neutrophils begin to stick to the inner surface of the
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endothelium of blood vessels. Then neutrophils begin to squeeze through the wall of the blood vessel to reach the damaged area. Process called emigration. XIII. Leukocytosis: increase in WBC’s in the blood XIV. Pus: collection of dead cells and fluid. XV. Fever: is an abnormally high body temperature that occurs because the hypothalamic thermostat is reset. It commonly occurs during infection and inflammation. Elevated body temperature INTENSIFIES the effects of interferons, inhibits the growth of microbes, and speeds up body reactions that aid repair.
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  • cells, Cytotoxic T cells

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