Chapter 17 Inflammation And Immunity

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SELF TOLERANCE

Back 1

Recognizing self versus non self which is necessary to prevent healthy body cells from being destroyed along with the invaders

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NEUTROPHILS

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Provides protection after invaders especially bacteria enter the body. Only mature cells are capable of phagocytosis. So the higher the numbers of mature neutrophils the greater the resistance to Infection .

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LEFT SHIFT

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Indicated that the patients bone marrow cannot produce enough mature neutrophils to keep pace with the continuing Infection and is releasing immature neutrophils into the body.

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MACROPHAGES

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Are important in immediate inflammatory responses and also stimulate the longer lasting immune response and antibody mediated immunity and cell mediated immunity. Can easily distinguish between self and non self

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BASOPHILS

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Cause the manifestations of inflammation. They act on blood vessels with basophil chemicals which include heparin, histamine, serotonin, kinins, and leukotriens. They stimulate both general inflammation and the inflammation of allergy and hypersensitivity reactions.

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EUSINOPHILS

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Very active against parasitic larvae and also limits inflammatory reactions.

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5 CARDINAL MANIFESTATIONS OF INFLAMMATION

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Warmth, Redness, swelling, pains, and decreased function.

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Sequence of inflammation

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1) vascular part. These blood vessel changes cause Redness and warmth of the tissues. The increased blood flow increases delivery of nutrients to injured tissues. Macrophages are the main cell involved in this stage.

2) cellular exudate. Exudate in the form of pus containing dead WBCs necrotic tissue, and fluids that escape from damaged cells.

3) Tissue repair and replacement. Scar tissue is formed causing function loss.

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AGGLITINATION

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Clumping action that results from the antibody linking antigens together. It slows the movement of the antigen into body fluids.

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Complement activation

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Activations triggered by the IgG and IgM classes of antibodies that can remove or destroy and antigen.

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Precipitation

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Antibody molecules bind so much antigen together that large antigen-antibody complexes are formed.

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IgA Antibody

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Secretory antibody that is present in high concentrations in the secretions of mucous membranes and in the Intestinal mucosa. Most responsible for preventing Infection in the upper and lower Respiratory tracts, the GI and GU tracts.

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IgD Antibody

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Present in low blood concentrations in conjunction with IgM

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IgE Antibody

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Associated with antibody mediated hypersensitivity reactions. Binds to mast cells and causes their degranulation when an allergen binds to IgE antigen recognition sites.

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IgG Antibody

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Provides sustained long term immunity against invading organisms. Activates classic complement pathway and enhances neutrophil and macrophages actions.

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IgM Antibody

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The first antibody formed by a newly sensitized B-lymphocyte plasma cell. Especially effective at the antibody actions of agglutination and precipitation because of having 10 potential binding sites per molecule. Activates complement pathway.

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ACQUIRED IMMUNITY

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Occurs either naturally or artificially through lymphocyte responses and cab be either active or passive.

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ACTIVE IMMUNITY

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Occurs when antigens enter a person's body and it responds by making specific antibodies against the antigen. The body takes an active part

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Natural active immunity

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Occurs when an antigen enters the body naturally without human assistance and the body responds by actively making antibodies against that antigen. Is the most effective and longest lasting immunity.

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PASSIVE IMMUNITY

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Occurs when the antibodies of an antigen are transferred to a person's body after first being made in the body of another person or animal. EX. Patients exposed to snake bite, rabies, tetanus,

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CYTOKINES

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Small protein hormones produced by the many WBCs. They work like hormones; one cell produces a cytokine which in turn exerts its effects on other cells of the immune system. They act like messengers that tell specific cells how and when to respond.

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INTERLEUKIN 1

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*Induces fever

*stimulates production of prostaglandins

*Increases growth of CD4+ T cells

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INTERLEUKIN-2

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*Increases growth and stimulation of T-ymphocytes

*enhances natural killer cell activity against cancer cells

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INTERLEUKIN-6

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*Stimulates liver to produce fibrinogen and protein C

* increases rate if bone marrow production of stem cells.

*Increases numbers of sensitized B-ymphocytes.

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TUMOR NECROSIS FACTOR (TNF)

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*Induces fever

* major cytokine involved in rheumatoid arthritis

*Major cytokine involved in the acute inflammatory response to infectious bacteria

*Participates in graft rejection

* Induces cell death

*Stimulates delayed hypersensitivity reactions and allergy.

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HYPER- ACUTE REJECTION

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Begins immediately on transplantation and is an antibody mediated response. Wide spread clotting in the transplanted organ occurs causing NECROSIS. The process cannot be stopped once it has started and the rejected organ is removed as soon as this is diagnosed.

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ACUTE REJECTION

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First occurs within 1 week to 3 months. Drug management of the patients immune response may limit damage to the organ and allow the graft to be maintained.

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CHRONIC REJECTION

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The donated organ tissues are replaced with fibrotic scale-like tissue. There is no cure for chronic graft rejection