Leukotrienes Leukotrienes are released when the mast cell degranulates They are

Leukotrienes leukotrienes are released when the mast

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Leukotrienes Leukotrienes are released when the mast cell degranulates. They are also known as slow reaction substances of anaphylaxis (SRS-A) and tend to prolong the inflammatory response. *important for later stages of inflammation* They cause vasodilation, smooth muscle contration, and attract neutrophils, monocytes and eosinophils. This is the target of inhibition for the drug Singulair Prostaglandins Prostaglandins are also released when the mast cell degranulates and are produced by the arachidonic pathway. But ultimately, they function to cause vasodilation, platelet aggregation at the site of injury, pain and fever AKA reaction substances of anaphylaxis (SRS-A Chemotactic Factors Attract neutrophils, eosinophils, and (Monocytes that turn into Macrophages once inside injured tissue). All of these perform phagocytosis. Platelet Activating Factor -Derived from mast cell -Produced by removal of a fatty acid from the plasma membrane & produced during inflammation by neutrophils, monocytes, endothelial cells, platelets -Similar to leukotrienes (causes endothelial cell retraction to increase vascular permeability, leukocyte adhesion to endothelial cells, platelet activation) Neutrophils Neutrophils will show up at the site of injury in 6-12 hours are responsible for phagocytosis. * First responders* ingest bacteria, dead cells, cellular debris -Short lived (mature cell, cannot divide, sensitive to acidic environment) >
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becomes component of purulent exudate/pus > removed from through epithelium or lymphatic system **Removal of debris in sterile lesions (burns) & phagocytosis of bacteria in nonsterile lesions** Monocytes Monocytes will show up in 1-7days, and are responsible for phagocytosis. Monocytes become Macrophages when they enter the tissue . they are responsible for “presenting antigens” to the T-helper cell which triggers T-cell immunity and the T-cell immunity goes on to trigger B-cell immunity. Also Monocytes release the following cytokines : IL1 causes fever, activates phagocytes & lymphocytes and also increases the release of IL 6 IL6 stimulates the production of acute phase reactants and promotes the growth and stimulation of blood cells. TNF can cause fever, increases the synthesis of proinflammatory proteins by the liver, causes muscle wasting and induces thrombosis. Growth Factors promote the production and maturation of neutrophils. Complement May destroy pathogens directly & activate/collaborate with any other component of inflammatory system (Proteins in this system=body’s most potent defenders, especially against bacterial infection) Complement- functions include: bacterial lysis, vasodilation and increase vascular permeability, (sepsis*) triggers mast cell degranulation = activation of 4 acute phase reactants chemotaxis opsonization (opsonin- molecules that “tag” microorganisms for destruction by cells of inflammatory system- neutrophils/macrophages) Kinin Kinin is turned into bradykinin which is responsible for: pain, chemotaxis, increase vascular permeability and vasodilation (sepsis*)
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