30 BIO 326R Inflammation Hypersensitivity Complement

30 BIO 326R Inflammation Hypersensitivity Complement - BIO...

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BIO 326R Inflammation, Hypersensitivity, Complement
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Acute inflammation A nonspecific response to tissue injury from trauma, infection Classic signs of Redness (rubor) Warmth (calor) Pain (dolor) Swelling (tumor) Injured tissue releases chemicals to nearby capillaries/endothelial cells (endothelial cells are cells which line blood vessels). Endothelial cells will increase expression of selectins . Selectins are Cell Adhesion Molecules (CAMs). Leukocytes (WBCs), adhere to selectins, but not tightly. Thus, they often roll along the capillary walls rather than flow through the blood stream. The increased number of selectins will cause them to slow down or even stop. The adherent WBCs (primarily neutrophils) are then exposed to the inflammatory chemicals and may become activated and then express integrins , which causes them to stop rolling. The neutrophils may then squeeze through the capillaries and migrate to the site of tissue injury. .
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Acute inflammation Factors released by the injured tissue as well as pathogens may act as chemotactic factors, attracting more leukocytes. The nature of the injury or pathogen may cause different types of attraction (e.g. bacterial infection attracting neutrophils, viral infection attracting NK cells). Tissue injury may also lead to a decrease in pH, which activates kallikrein , an extracellular protease. Kallikrein cleaves bradykinin precursor to release active bradykinin peptides Bradykinin will act at the capillary walls, opening the junction between endothelial cells, allowing greater access to more leukocytes and fluid from blood (including complement molecules) and bind to mast cells, causing release of histamine (vasodilator) and heparin (anticoagulant). Vasodilation increases permeability of the capillaries, allowing fluid from blood to accumulate at site of injury (swelling). Other molecules which are produced or released Nerve cells release substance P, which will also cause histamine release from mast cells Arachidonic acid is released from many cells and metabolized into prostaglandins (vasodilator and pain stimulant) and other pro-inflammatory molecules (pain). NSAIDs (N on-S teroidal A nti-Inflammatory D rugs (Aspirin, ibuprofen, naproxen etc.)) act by preventing formation of prostaglandins Massive vasodilation, degradation of membranes, inhibition of clotting, activation of many cells, stimulation of pain receptors = “inflammation” TLRs: Toll Like Receptors. Receptors on some immune cells, specialized for binding (mostly) foreign substances, such as LPS, peptidoglycan, RNA etc.
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Injury with bacterial infection Release of inflammatory signals from dead cells (RNA, cellular proteins) Kallikrien activation Cleavage and activation of bradykinin H+ pH drops Bacteria : LPS, peptidoglycan, flagellin, carbohydrates Binding to TLRs causes Release of numerous cytokines B K K Inactive Active Active bradykinin subunit B
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This note was uploaded on 07/24/2009 for the course BIO 52035 taught by Professor Edsatterwhite during the Spring '08 term at University of Texas at Austin.

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30 BIO 326R Inflammation Hypersensitivity Complement - BIO...

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