Chapter 10.docx

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Department
Kinesiology & Health Science
Course
KINE 2011
Professor
Olivier Birot
Semester
Fall

Description
Chapter 10: Body Defenses Introduction - Immunity: the body’s ability to resist/eliminate potentially harmful foreign materials or abnormal cells o State of protection from infectious disease - Immune system: internal defence system that recognizes and destroys/neutralizes materials within the body that are foreign to the “normal self” o Defends against invading pathogens (ex: bacteria, viruses) o Removes worn-out cells damaged by trauma or disease; facilitates wound healing and tissue repair o Immune surveillance - identifies and destroys abnormal/mutant cells that have originated in the body (chief internal defence mechanism against cancer) o Mounts inappropriate immune response that lead to allergies (when the body turns against a normally harmless environmental chemical entity) or to autoimmune diseases (when the defence system erroneously produces antibodies against a particular type of the body’s own cells) o Exercise is the only action that has proven to have a profound effect on the acute and chronic functioning of the immune system Targets of Immune System - Virulence: disease producing power of a pathogen - Bacteria – large, self-sustaining o Non-nucleated, single-celled microorganisms o Pathogenic bacteria: cause tissue damage and produce disease by releasing enzymes/toxins that physically injure/functionally disrupt affected cells and organs o Ex: TB, tetanus, whooping cough - Viruses – small, not self-sustaining (consist only of nucleic acids in a protein coat; can’t reproduce unless that invade a host cell and take over its biochemical facilities) o Body’s own defence system will see the host cell as foreign and may destroy the virus by destroying the host cell itself o Can deplete essential cell components, dictating that the host cell produce substances toxic to it o Can turn the cell cancerous o Common viruses: SARS, H1N1, avian (bird) flu, polio, influenza, measles, AIDS  Can be spread over large distances via world travel - Fungi – can be multicellular; often cause disease of the skin/epithelium o Ex: thrush, ringworm - Parasites – multicellular; have different forms/habitats at different stages of their life cycle o Ex: malaria, leishmaniasis Leukocytes - Leukocytes = effectors of the immune system o Neutrophils, eosinophils, basophils, monocytes, lymphocytes (B and T cells) o Use the blood and lymphatic vessel system to travel to the site of action where they are needed; their means of surveillance  Site of action = where the infectious agents are OR in the secondary lymphoid tissue where they produce/secrete active factors to fight the infectious agents - Lymphoid tissues: the tissues that produce, store or process lymphocytes o Strategically located to intercept invading microorganisms before they have a chance to spread very far  Primary lymphoid tissue (where cells develop)  Bone marrow: origin of all blood cells, site of maturational processing for B lymphocytes  Thymus: site of maturational processing for T lymphocytes, secretes the hormone thymosin  Secondary lymphoid tissue (where cells develop and mature into specific functioning immune cells; are stored until needed)  Lymph nodes/appendix/Peyer’s patches or “gut-associated lymphoid tissue” (GALT)/tonsils/adenoids: exchanges lymphocytes with the lymph, resident lymphocytes produce antibodies and sensitized T cells which are released into the lymph, resident macrophages remove microbes and other debris from the lymph  Spleen: exchanges lymphocytes with the blood, resident lymphocytes produce antibodies and sensitized T cells which are released into the blood, resident macrophages remove microbes and other debris (ex: worn out red blood cells) from the blood, stores a small percentage of red blood cells which can be added to the blood by splenic contractions if needed Immune Responses - Two systems work together generate immunity – innate and adaptive - Innate (built-in) immune system: o Nonspecific o Responses work immediately when body is exposed to a threatening agent o Nonselectively defends against foreign invaders o First line of defence o Rapid but limited responses (last about a week) o Neutrophils, macrophages and several groups of plasma proteins are especially important here - Adaptive/acquired immune system: characterized by memory and specificity o Specifically targets foreign material to which the body has already been exposed o Body has taken time to prepare to attack (takes longer than innate immunity to become effective) o The ultimate weapon against pathogens o Responses are mediated by B and T lymphocytes  Each individual one can recognize and defend against only one particular type of foreign material  When this material is identified in the body, only the lymphocyte specific to that pathogen is called to action o It multiplies so that a highly targeted attack can be launched  Collection of activate and expanded T and B cells constantly changes in response to the pathogens in the body at a given time o Formation of memory cells allows system to react more swiftly against specific invaders in the future Innate Adaptive Response Time Hours Days Specificity Limited and fixed Highly diverse, improves during the course of the immune response Response to Identical to primary Much more rapid than primary response Repeat Infection response (because of memory cells) Major Barriers (ex: skin), Lymphocytes, antigen-specific receptors, Components phagocytes, pattern antibodies recognition molecules Innate Immunity Inflammation - Nonspecific response to tissue injury - Neutrophils and macrophages (phagocytes) play a major role - Goal – to bring phagocytes and plasma proteins to the invaded/injured area. These: o Isolate, destroy or inactivate invaders o Remove debris o Prepare for subsequent healing and repair - Inflammation is not a synonym for infection o Infection is caused by an exogenous pathogen  Inflammation can be caused by infection – is the response of the organism to the pathogen  Can also be caused by things other than infection (ex: trauma) Typical sequence of events during an inflammatory response: - Bacterial invasion/tissue damage o Release of histamine by mast cells  Local arteriolar vasodilation  Increased blood delivery to injured tissue o Redness + heat  Increase in crucial plasma proteins, such as clotting factors, in tissue  Defence against foreign invader, tissue repair  Increased local capillary permeability  Local accumulation of fluid (oedema) o Swelling + pain  Increase in phagocytes in tissue  Defence against foreign invader, tissue repair  Phagocytic secretions o Systemic response (ex: fever) Similar Inflammatory Response Regardless of Trigger - Defence by resident tissue macrophages – when bacteria get in through a break in the skin, macrophages that are already at the invaded site start to phagocytize them o They secrete active chemicals/factors - Localized vasodilation – immediately upon invasion, arterioles within the area dilate, soon after capillaries follow o Brings more blood to the area which brings more phagocytic leukocytes and plasma proteins - Increased capillary permeability – caused by release of histamine enlarging the capillary pores (space between endothelial cells) o Allows plasma protein to leave the blood and get into the inflamed tissue - Localized oedema – local accumulation of fluid causes swelling and pain o Increases the # of leukocytic phagocytes and plasma proteins in affected areas - Walling of the inflamed area – on exposure to tissue thromboplastin in the injured tissue, fibrinogen is converted into fibrin o Fibrin forms interstitial fluid clots in the spaces around the bacterial invaders and damaged cells  Walls off the injured area, preventing/delaying the spread of bacterial invaders and their toxic products - Emigration of leukocytes – arrive within an hour after injury o Neutrophils come first; slower moving monocytes come within the next 8-12 hrs. o How leukocytes emigrate from the blood into the tissues:  Adhered leukocytes leave by diapedesis (squeeze out of a capillary pore in an amoeba-like fashion)  Leukocyte crawls toward affected area - Leukocyte proliferation - Marking of bacteria for destruction by opsonins (body-produced chemicals that make bacteria more susceptible to phagocytosis) – links the foreign cell and the phagocytic cell so that it can’t escape before phagocytosis occurs - Leukocytic destruction of bacteria – neutrophils and macrophages clear the inflamed area of infectious/toxic agents and tissue debris by phagocytic and nonphagocytic means o Clearing action for tissue repair = main function of inflammation o Pus: collection of living and dead phagocytic cells, dead tissue liquefied by lysosomal enzymes and bacteria in an infected wound - Mediation of the inflammatory response by phagocyte-secreted chemicals – o Macrophages secrete:  Nitric oxide – toxic to nearby microbes  Endogenous pyrogen (EP) – induces fever which is beneficial to the overall inflammatory response  Interleukin 1 (IL-1) – enhances proliferation and differentiation o
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