Leukotrienes
Cause increased permeability
Produced by basophils and mast cells.
During inflammation local temperature increases causing increased metabolic reactions which produces more heat. Edema results causing more fluid into tissue spaces. Pain results from injury to neurons and from toxic chemicals released by microbes.
2) Emigration of Phagocytes
Within 1 hour after the inflammation process begins phagocytes appear at the scene. Neutrophils begin to squeeze through the wall of the blood vessel to reach the damaged area. This is called Emigration . As the inflammation process continues, neutrophils die off quickly. Monocytes then follow the neutrophils into the affected area where they transform into wandering macrophages that add to the phagocytic activity. Eventually macrophages also die making a pocket of dead phagocytes called Pus.
3) Tissue Repair
Fibroblasts enter the site of damage and begin the repair process.
E) Fever
This is an abnormally high body temperature that occurs because the hypothalamic thermostat is reset. Many bacterial toxins elevate body temperature triggered by the release of fever- causing cytokines from macrophages. Fever intensifies the effects of Interferons, inhibits the growth of some microbes, and speeds up the body reactions that aid in repair.
Adaptive (Acquired) Immunity (Specific)
The ability of the body to defend itself against specific invading agents such as bacteria, toxins, viruses, and foreign tissues.
Anitgens (Ags): substances recognized as foreign and provoke immune responses.
Differences between Adaptive and Innate Immunity are:
Specificity for particular foreign molecules (antigens) which also distinguishes “self” from “non-self” molecules. Memory for most previously encountered antigens so that a second encounter prompts an even more rapid and vigorous response Time is required between exposure & activity The body must be exposed to the pathogen before immunity develops The body must acquire immunity (passive or active)
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