Inflammation

April 14, 2009. The Immune response to a break in the skin. Phagocytosis occurs:
Chemotaxis-chemically stimulated movement of phagocytes to the area of the break in the skin. Phagocyte binds to microbe. Pseudopods extend from the plasma membrane and engulf the microbe, when the pseudopods meet they surround the microbe with a sac called a phagosome. The phagosome meets a lysosome in the cytoplasma and they merge becoming a phagolysosome. The phagolysosome releases digestive enzymes and oxidants that quickly kill many types of microbes. Inflammation is a non-specific immune response. The signs and symptoms associative with inflammation: 1. Is swelling-edema where vasodilation increases fluid to the area and it leaks into the nearby tissue, 2. Then there is pain because of the excess fluid in the surrounding tissue is putting pressure on the sensory neurons. 3 & 4. There is redness/higher temperature because of the extra blood flow to the region of the break in the skin. The are 3 basic stages to the inflammatory response: 1. Vasodilation, 2. Movement of phagocytes from blood into interstitial fluid, and 3. Tissue repair. This happens in the first 3 days of damage.
The everyday use of aspirin and ibuprofen blocks the COX 1 and COX 2 enzymes. COX1 is responsible for baseline of prostaglandins. COX 2 produces prostaglandins through stimulation. Prostaglandins are produced from mast cells and are a group of lipids that case vasodilation. COX 1 and COX 2 are 2 enzymes that take the fatty acid tails of Arachodonic acid to prostaglandins. Arachodonic acid is the precursor for production of signaling molecules. Blocking these with aspirin and NSAID’s can cause the healing process to slow.