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Innate Immunity Inflammation PowerPoint Presentation

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Chapter 7 Innate Immunity: Inflammation
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Immunity Types of immunity Innate resistance: Natural barriers and the inflammatory response Adaptive (acquired) immune system Lines of defense First line Natural barriers: Skin and mucous membranes Second line Inflammation Third line Adaptive (acquired) immunity
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First Line of Defense Physical and mechanical barriers Skin and low skin temperature Linings of the gastrointestinal, genitourinary, and respiratory tracts Highly interconnected junctions Sloughing off of cells Coughing and sneezing “Washing” Vomiting Urinating Mucus and cilia
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First Line of Defense (cont’d) Biochemical barriers Synthesize and secrete substances to trap or destroy microorganisms Antibacterial peptides in mucus, perspiration (sweat), saliva, tears, and earwax Antimicrobial peptides Cathelicidins, defensins (α defensins in neutrophil granules and β defensins), and collectins (lungs) Normal microbiome Inhibits colonization by pathogens; releases chemicals that prevent infection Vaginal: Lactobacillus Intestinal: Ammonia, phenols, and indoles
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Second Line of Defense Inflammatory response Causes Infection, mechanical damage, ischemia, nutrient deprivation, temperature extremes, and radiation Cellular and chemical components Nonspecific Takes place in approximately the same way, regardless of the type of stimulus or whether exposure to the same stimulus has occurred in the past Rapidly initiated No memory cells
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Second Line of Defense (cont’d) Inflammatory response (cont’d) Cardinal signs Redness, heat, swelling, and pain Vascular response Blood vessel dilation, increased vascular permeability and leakage, white blood cell (WBC) adherence to the inner walls of the vessels, and migration through the vessels (diapedesis)
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Second Line of Defense (cont’d) Inflammatory response (cont’d) Once in the tissues, the cells and chemicals associated with the inflammatory response: Limit and control the inflammatory process. Prevent and limit infection and further damage. Interact with components of the adaptive immune system. Prepare the area of injury for healing.
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Second Line of Defense (cont’d) Question 1 The characteristic vascular changes at the site of an injury produce: Blood vessel constriction after dilation Increased permeability and leakage Tightening of the capillary endothelial cell junctions Pallor and swelling where the injury occurred
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Plasma Protein Systems Protein systems that provide a biochemical barrier against invading pathogens are the: Complement system Clotting system Kinin system All contain inactive enzymes (proenzymes). Sequentially activated–cascade First proenzyme is converted to an active enzyme. The activation of the first component of a system results in sequential activation of other components.
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Plasma Protein Systems (cont’d) Complement system Can destroy pathogens directly Activates or collaborates with every other component of the inflammatory response Pathways Classical: Antibody and antigens Lectin: Mannose-containing bacterial carbohydrates Alternative: Gram-negative bacterial and fungal cell wall polysaccharides Functions Anaphylatoxic activity resulting in mast cell degranulation; leukocyte chemotaxis; opsonization; cell lysis
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Plasma Protein Systems (cont’d) Clotting (coagulation) system Forms a fibrinous mesh at an injured or inflamed site Prevents the spread of infection. Keeps microorganisms and foreign bodies at the site of inflammation for removal. Forms a clot that stops the bleeding. Provides a framework for repair and healing. Main substance is an insoluble protein called fibrin Pathways Extrinsic: Is activated by the tissue factor outside the vascular space. Intrinsic: Is activated in the vascular space when the vessel wall is damaged.
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Plasma Protein Systems (cont’d) Kinin system Functions to activate and assist inflammatory cells. Kinin is primarily bradykinin. Causes dilation of blood vessels, pain, smooth muscle contraction, vascular permeability, and leukocyte chemotaxis. Kininases degrade kinins.
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Plasma Protein Systems (cont’d) Interactions among the three plasma protein systems are finely regulated to prevent injury to the host tissue and to guarantee activation when needed. Multiple mechanisms are available to either activate or inactivate (regulate) these plasma protein systems. Plasmin-activates mechanism Hageman factor–activates mechanism Together, both of these mechanisms activate the clotting cascade, the complement system, and the kinin proteins.
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Plasma Protein Systems (cont’d)
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Plasma Protein Systems (cont’d) Interactions among the three plasma protein systems control inflammation and inhibit the three plasma protein systems. Carboxypeptidase—Inhibits C3a and C5a Histaminase—Inhibits histamine Arylsulfatase—Inhibits histamine Kinases—Inhibits kinins C1 esterase inhibitor—Inhibits complement
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Cellular Mediators of Inflammation Cellular mediators Mast cells Granulocytes (neutrophils, eosinophils, basophils) Monocytes and macrophages Natural killer (NK) cells and lymphocytes Cellular fragments (platelets) Biochemical mediators Are responsible for vascular changes. Modulate the localization and activities of other inflammatory cells. Include histamine, chemotactic factors, leukotrienes, prostaglandins, and the platelet-activating factor.
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Cellular Mediators of Inflammation (cont’d) Mast cells are the most important activators of inflammation. Cell surface or cellular receptors Pattern recognition receptors (PRRs) Toll-like receptors (TLRs): Recognize pathogen-associated molecular patterns (PAMPs). Complement receptors: Recognize complement fragments. Scavenger receptors: Promote phagocytosis. PAMPs Damage-associated molecular patterns (DAMPs) Inflammatory response Is initiated when tissue injury occurs or when PAMPs are recognized by PRRs on cells of the innate immune system.
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Cellular Mediators of Inflammation (cont’d) Cellular products Chemokines or cytokines: Regulate innate or adaptive resistance by affecting other neighboring cells. Are either proinflammatory or antiinflammatory. Actions are pleiotropic: The same molecule may have a large variety of different biologic activities, depending on the particular target cell to which it binds. Are either synergistic or antagonistic. Include interleukins, interferons, and tumor necrosis factor (TNF).
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Cytokines Interleukins (ILs) Are produced primarily by macrophages and lymphocytes in response to a microorganisms or stimulation by other products of inflammation. Help regulate inflammation. Many types exist. Examples IL-1 is a proinflammatory cytokine: Causes fever. IL-6 is a proinflammatory cytokine: Helps with healing. IL-10 is an antiinflammatory cytokine. Transforming growth factor–beta (TGF-β) is an antiinflammatory cytokine.
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Cytokines (cont’d) Interferons (INFs) Protects against viral infections. Is produced and released by virally infected host cells in response to viral double-stranded ribonucleic acid (RNA). Does not directly kill viruses but prevents them from infecting additional healthy cells. Types INF-α and INF-ß Induce the production of antiviral proteins. INF-ϒ Increases microbiocidal activity of macrophages.
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Cytokines (cont’d) Interferon actions
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Cytokines (cont’d) TNF-α Is secreted by macrophages in response to PAMP by TLR recognition. Produces local and systemic effects. Induces fever by acting as an endogenous pyrogen. Increases synthesis of proinflammatory proteins. Causes muscle wasting (cachexia) and intravascular thrombosis. Is probably responsible for fatalities from shock caused by gram-negative bacterial infections.
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Chemokines Induce WBC chemotaxis. Are produced by macrophages, fibroblasts, and endothelial cells. More than 40 different kinds exist. Vast majority are classified as either CC-chemokines (β-chemokines) or CXC-chemokines (α-chemokines). CC-chemokines affect mainly monocytes, lymphocytes, and eosinophils. CXC-chemokines generally affect neutrophils.
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Mast Cells Are cellular bags of granules located in loose connective tissues close to blood vessels. Skin, digestive lining, and respiratory tract Activation Physical injury, chemical agents, immunologic processes, and TLRs Chemicals are released in two ways: Degranulation Synthesis of lipid-derived chemical mediators
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Mast Cell Degranulation Releases histamine Causes temporary and rapid constriction of the large blood vessels and dilation of the postcapillary venules. Endothelial cells that line the capillaries are retracted. Receptors H1 receptor (proinflammatory): Is present in smooth muscle cells of the bronchi. Induces bronchoconstriction. H2 receptor (antiinflammatory): Is present on parietal cells of the stomach mucosa. Induces the secretion of gastric acid.
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Mast Cell Degranulation (cont’d) Chemotactic factors Neutrophil chemotactic factor Attracts neutrophils. Eosinophil chemotactic factor of anaphylaxis (ECF-A) Attracts eosinophils.
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Mast Cell Synthesis of Mediators Leukotrienes Are the product of arachidonic acid from mast cell membranes. Have similar effects to histamine. Are more important in the later stages of inflammation. Prostaglandins Have similar effects to leukotrienes; they also induce pain. Platelet-activating factor Effect is similar to leukotrienes; they also activate platelets.
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Mast Cells Question 2 Which statement indicates the nurse has an accurate understanding of mast cells? Mast cells: “Can be activated through an intrinsic or extrinsic pathway.” “Degranulate in response to chemical agents.” “Reduce blood flow after activation.” “Can be blocked by the therapeutic use of aspirin.”
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Endothelium Maintains normal blood flow. Endothelial cells produce nitric oxide (NO) and prostacyclin (PGI2). NO and PGI2 maintain blood flow and pressure and inhibit platelet activation. NO maintains vascular tone. During inflammation, the endothelium Expresses receptors that help leukocytes leave the circulation. Retracts to allow fluid to pass into the tissues. Damage to endothelium promotes clotting.
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Platelets Are cellular fragments formed from megakaryocytes. Platelets are also called thrombocytes. Activation of platelets stops bleeding and degranulation. Platelets contain alpha and dense granules.
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Phagocytes Neutrophils Are also referred to as polymorphonuclear neutrophils (PMNs). Predominate in early inflammatory responses. Ingest bacteria, dead cells, and cellular debris. Are short lived and become components of the purulent exudate (pus). Primary roles Removal of debris in sterile lesions Phagocytosis of bacteria in nonsterile lesions
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Phagocytes (cont’d) Eosinophils Provide the defense against parasites and regulate vascular mediators. Help control vascular effects of inflammation. Basophils Are similar to but are not mast cells. Are an important source for cytokine IL-4. Are associated with allergies and asthma. Their role is uncertain.
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Phagocytes (cont’d) Monocytes and macrophages Monocytes that are produced in the bone marrow, enter circulation, migrate to the inflammatory site, and develop into macrophages. Monocytes are precursors to macrophages in tissues Kupffer cells (liver); alveolar macrophages (lungs); and microglia (brain) Macrophages are larger than monocytes, are more active than phagocytes, and are important cellular initiators of inflammation; they help in wound healing. Activation results in increased phagocytic activity, size, plasma membrane area, glucose metabolism, and number of lysosomes; they predominate in late inflammation.
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Phagocytes (cont’d) NK cells: Recognize and eliminate cells that are infected with viruses and cancer cells in the blood. Lymphocytes: Are the main component of the adaptive immune response.
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Phagocytosis Is the process by which a cell ingests and disposes of foreign material. Is the destruction of microorganisms and cellular debris. Production of adhesion molecules occurs. Margination (pavementing) occurs. Leukocytes adhere to endothelial cells. Diapedesis occurs. Cells emigrate through the endothelial junctions.
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Phagocytosis (cont’d) Steps Opsonization (“glue” between the phagocyte and the target cell by C3b making the foreign cell more susceptible to phagocytosis), recognition, and adherence Engulfment Small pseudopods surround adherent microorganism. Phagosome formation Fusion with lysosomal granules Creates a phagolysosome. Destruction of the target Uses primary and secondary granules.
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Phagocytosis (cont’d) Respiratory burst Oxygen-dependent killing mechanism α1-antitrypsin Helps minimize the destructive effects of the enzymes released by the dying phagocytes.
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Phagocytosis (cont’d) Question 3 Which information is correct regarding phagocytosis? Phagocytosis requires: Digestion of the capillary basement membrane during diapedesis A reduction in nitric oxide production Formation of a phagosome by a mast cell A respiratory burst produced by the release of the primary lysosomal granules
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Local manifestations of inflammation result from vascular changes and corresponding leakage of circulating components into the tissue. Heat: From vasodilation and increased blood flow Redness: From vasodilation and increased blood flow Swelling: From exudate accumulations and fluid from capillary permeability Pain: From pressure exerted by exudate accumulations, prostaglandins, and bradykinins Loss of function: May also occur Local Manifestations of Inflammation
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Local Manifestations of Inflammation (cont’d) Functions Dilute toxins. Carry plasma proteins and leukocytes to the injury site. Carry bacterial toxins and debris away from the site.
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Exudative Fluids Exudate: Fluid and cells, such as protein and debris Serous exudate Watery exudate: Indicates early inflammation. Fibrinous exudate Thick, clotted exudate: Indicates more advanced inflammation. Purulent (suppurative) exudate Pus: Indicates a bacterial infection. Hemorrhagic exudate Exudate containing blood: Indicates bleeding.
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Systemic Manifestations of Inflammation Fever Caused by exogenous and endogenous (IL-1) pyrogens Acts directly on the hypothalamus Leukocytosis Increased numbers of circulating leukocytes Left shift, increase in immature cells (bands) Increased plasma protein synthesis Acute-phase reactants C-reactive protein, fibrinogen, haptoglobin, amyloid A, and ceruloplasmin
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Chronic Inflammation Is inflammation that lasts from 2 weeks to months to years. Is often related to an unsuccessful acute inflammatory response. Other causes High lipid and wax content of a microorganism Ability to survive inside the macrophage Toxins Chemicals, particulate matter, or physical irritants
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Chronic Inflammation (cont’d) Characteristics Dense infiltration of lymphocytes and macrophages Granuloma formation Epithelioid cell formation Giant cell formation
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Resolution and Repair Regeneration Most favorable outcome Resolution Returning injured tissue to the original structure and function Repair Replacement of destroyed tissue with scar tissue Scar tissue Primarily composed of collagen to restore the tensile strength of the tissue
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Resolution and Repair (cont’d) Débridement Cleaning up dissolved clots, microorganisms, erythrocytes, and dead tissue cells Healing Filling in the wound Sealing the wound (epithelialization) Shrinking the wound (contraction)
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Healing Primary Intention Wounds that heal under conditions of minimal tissue loss Original tissue structure and function that have been restored Secondary Intention Wounds that require significantly more tissue replacement Open wound Wounds the cause scar formation
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Healing (cont’d) Primary intention
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Healing (cont’d) Secondary intention
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Healing (cont’d) Question 4 A person has a large open wound that has formed scar tissue. The nurse knows which type of healing has occurred? Primary Secondary Débridement Regeneration
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Healing (cont’d) Reconstructive phase Wound begins to heal. Healing begins 3 to 4 days after the injury and continues for 2 weeks. Fibroblast proliferation occurs. Collagen synthesis by fibroblasts. Epithelialization–cells from healthy tissue grow into wound. Wound contracts through the actions of myofibroblasts. Cellular differentiation occurs.
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Healing (cont’d) Reconstructive phase (cont’d)
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Healing (cont’d) Maturation phase Healed wound is remodeled. This phase begins several weeks after injury and may last for 2 years. Cellular differentiation continues. Scar tissue forms. Scar remodeling occurs.
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Healing (cont’d) Maturation phase (cont’d)
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Dysfunctional Wound Healing Dysfunction during inflammatory response Hemorrhage Fibrous adhesion Infection Excess scar formation Wound sepsis Hypovolemia Hypoproteinemia Antiinflammatory steroids
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Dysfunctional Wound Healing (cont’d) Dysfunction during reconstructive phase Impaired collagen matrix assembly Causes: Malnutrition Keloid scar Hypertrophic scar Impaired epithelialization Antiinflammatory steroids, hypoxemia, and nutritional deficiencies Cleaning with povidone-iodine and hydrogen peroxide Impaired contraction Contractures: Results from excessive myofibroblast-derived tension
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Dysfunctional Wound Healing (cont’d) Keloids
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Dysfunctional Wound Healing (cont’d) Wound disruption Dehiscence Wound pulls apart at the suture line. Causes: Excessive strain, wound sepsis, and obesity Occurs 5 to 12 days after suture. Characteristics Serous drainage is increased. Feels like something “gave way.” Surgery is required.
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Pediatrics and Mechanisms of Self Defense Neonates: Have transiently depressed inflammatory and immune function. Have neutrophils that are not capable of efficient chemotaxis. Have a deficient complement system. Are deficient in collectins and collectin-like proteins. Are susceptible to bacterial infections.
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Aging and Mechanisms of Self Defense Impaired or delayed inflammation is likely a result of chronic illness. Diabetes and cardiovascular disease, among others Medications may interfere with wound healing. Infections are more common in older adults. Lungs, urinary tract, and skin are often affected. Older adults have diminished immune function. Expression and function of several, if not all, TLRs, are decreased.