non specific host defenses
•Descargar como PPTX, PDF•
22 recomendaciones•9,934 vistas
non specific host defenses
Recomendados
Más contenido relacionado
La actualidad más candente
La actualidad más candente (20)
Destacado
Similar a non specific host defenses
Similar a non specific host defenses (20)
Último
Último (20)
non specific host defenses
- 1. Non-specific Host Defenses Prepared by: GEORGINE L. MANANTAN, RMT,RN,RM,MSN
- 3. Resistance Ability to ward off disease. The capacity of an organism to defend itself against a disease. The capacity of an organism or a tissue to withstand the effects of a harmful environmental agent.
- 4. Nonspecific Resistance: Defenses that protect against all pathogens. Specific Resistance: Protection against specific pathogens.
- 5. Susceptibility: Vulnerability or lack of resistance. the state of being predisposed to, sensitive to, or of lacking the ability to resist a pathogen, familial disease, or a drug.
- 7. First Line of Defense: Non-specific natural barriers which restrict entry of pathogen. Examples: Skin and mucous membranes.
- 8. Second Line of Defense: Innate non-specific immune defenses provide rapid local response to pathogen after it has entered host. Examples: Fever, phagocytes (macrophages & neutrophils), inflammation, and interferon.
- 9. cells
- 10. Third line of defense: Antigen-specific immune responses, specifically target and attack invaders that get past first two lines of defense. Examples: Antibodies and lymphocytes.
- 11. antibodies
- 13. Three Lines of Defense Against Infection
- 14. First Line of Defense: Skin and Mucous Membranes
- 15. I. Mechanical Defenses 1. Skinhas two Layers: A.Epidermis Thin outer layer of epithelial tissue. Contains Langerhans cells, dead cells, and keratin
- 16. B. Dermis Thick inner layer of connective tissue. Infections are rare in intact skin. Exceptions: Hookworms can penetrate intact skin Dermatophytes: “Skin loving” fungi
- 17. Intact Skin is an Effective Barrier Against Most Pathogens
- 18. I. Mechanical Defenses 2. Mucous Membranes Line gastrointestinal, genitourinary, and respiratory tracts.
- 19. Two layers: Outer epithelial and inner connective layer. Epithelial layer secretes mucus which maintains moist surfaces. Although they inhibit microbial entry, they offer less protection than skin.
- 20. Several microorganisms are capable of penetrating mucous membranes: •Papillomavirus •Treponema pallidum •Enteroinvasive E. coli •Entamoeba histolytica
- 21. Papillomavirus
- 23. Entamoeba coli Entamoeba histolytica
- 24. I. Mechanical Defenses 3. Lacrimal apparatus Continual washing and blinking prevents microbes from settling on the eye surface.
- 26. 4. Saliva Washes microbes from teeth and mouth mucous membranes. 5. Mucus Thick secretion that traps many microbes.
- 27. 6. Nose Hair Coated with mucus filter dust, pollen, and microbes.
- 28. 7. Ciliary Escalator Cilia on mucous membranes of lower respiratory tract move upwards towards throat at 1-3 cm/hour.
- 29. 8. Coughing and sneezing: Expel foreign objects.
- 31. Epiglottis Protects Respiratory System from Infection During Swallowing
- 32. 10. Urination Cleanses urethra. 11. Vaginal Secretions: Remove microbes from genital tract.
- 33. B. Chemical Defenses: Sebum: Oily substance produced by sebaceous glands that forms a protective layer over skin. Contains unsaturated fatty acids which inhibit growth of certain pathogenic bacteria and fungi.
- 34. pH Low, skin pH usually between 3 and 5. Caused by lactic acid and fatty acids.
- 35. Perspiration: Produced by sweat glands. Contains lysozyme and acids.
- 36. Lysozyme Enzyme that breaks down gram-positive cell walls. Found in nasal secretions, saliva, and tears.
- 37. B. Chemical Defenses Gastric Juice Mixture of hydrochloric acid, enzymes, and mucus. pH between 1.2 to 3 kills many microbes and destroys most toxins. Many enteric bacteria are protected by food particles.
- 38. Helicobacter pylori neutralizes stomach acid and can grow in the stomach, causing gastritis and ulcers.
- 40. Transferrins Iron-binding proteins in blood which inhibit bacterial growth by reducing available iron. also called Siderophilin, protein (beta1 globulin) in blood plasma that transports iron from the tissues and bloodstream to the bone marrow, where it is reused in the formation of hemoglobin.
- 41. Cellular Elements of Blood Cell Type # Cells/mm3 Function Erythrocytes (RBC) 4.8-5.4 million Transport O2 and CO2 Leukocytes (WBC) 5,000-10,000 Various A. Granulocytes: 1. Neutrophils (70% of WBC) Phagocytosis 2. Basophils (1%) Produce histamine 3. Eosinophils (4%) Toxins against parasites some phagocytosis B. Monocytes/Macrophages (5%) Phagocytosis C. Lymphocytes (20%) Antibody production (B cells) Cell mediated immunity (T cells) Platelets 300,000 Blood clotting
- 42. Composition of Human Blood
- 43. Platelets Form Blood Clots
- 44. II. Second Line of Defense
- 45. 1. Phagocytosis Derived from the Greek words “Eat and cell”. Phagocytosis is carried out by white blood cells: macrophages, neutrophils, occasionally eosinophils.
- 47. Wandering macrophages Originate from monocytes that leave blood and enter infected tissue, and develop into phagocytic cells.
- 48. Fixed Macrophages (Histiocytes): Located in liver, nervous system, lungs, lymph nodes, bone marrow, and several other tissues.
- 49. 1. Chemotaxis Phagocytes are chemically attracted to site of infection.
- 50. Phagocytic Cells: Macrophages (Monocytes), Neutrophils, and Eosinophils (Macrophages)
- 52. Phagocytes are Attracted to Site of Infection by Chemotaxis
- 53. 2. Adherence: Phagocyte plasma membrane attaches to surface of pathogen or foreign material. Adherence can be inhibited by capsules (S. pneumoniae) or M protein (S. pyogenes).
- 54. Opsonization: Coating process with opsonins that facilitates attachment. Opsonins include antibodies and complement proteins.
- 55. 3. Ingestion Plasma membrane of phagocytes extends projections (pseudopods) which engulf the microbe. Microbe is enclosed in a sac called phagosome.
- 56. 4. Digestion Inside the cell, phagosome fuses with lysosome to form a phagolysosome. Lysosomal enzymes kill most bacteria within 30 minutes and include: • Lysozyme: Destroys cell wall peptidoglycan • Lipases and Proteases • RNAses and DNAses After digestion, residual body with undigestable material is discharged.
- 58. Inflammatio nTriggered by tissue damage due to infection, heat, wound, etc.
- 59. Functions of Inflammation 1. Destroy and remove pathogens 2. If destruction is not possible, to limit effects by confining the pathogen and its products. 3. Repair and replace tissue damaged by pathogen and its products.
- 60. HOST DEFENSE
- 61. HOST DEFENSE POLYMORPHONUCLEAR LEUKOCYTES Neutrophils Eosinophils Basophils CELLULAR PARTICIPANTS
- 64. LYMPHOCYTES
- 66. PLATELETS
- 67. I n t e n s i t y Time Neutrophils Lymphocytes Macrophages Fibroblasts Fibrosis Acute Chronic Scar HOST DEFENSE INJURY REPAIR
- 71. Inflammation Major Symptoms of Inflammation: LOCAL MANIFESTATION 1. Redness 2. Pain 3. Heat 4. Swelling 5. Loss of function
- 73. • Leukocytosis (granulocytosis vs. lymphocytosis) • Elevated serum acute phase proteins (C-reactive protein, fibrinogen, etc) • Increased ESR (erythrocyte sedimentation rate) • Hypercoagulability ACUTE INFLAMMATION LABORATORY MANIFESTATIONS
- 74. ACUTE INFLAMMATION SEQUELAE INJURY RESOLUTION Autoimmune disease Chronic inflammation Acute inflammation Viral infection Chronic irritation Mediators Mediators
- 76. Vasoconstriction Vasodilation Increased vascular permeability Hemoconcentrati on and stasis Phagocytosis Leukocyte Adhesion Transmigration Chemotaxis Aggregation ACUTE INFLAMMATION SEQUENCE OF EVENTS
- 77. Stages of Inflammation 1. Vasodilation Increase in diameter of blood vessels. Triggered by chemicals released by damaged cells: histamine, kinins, prostaglandins, and leukotrienes.
- 80. Increasein Permeability Time ACUTE INFLAMMATION INCREASED VASCULAR PERMEABILITY Histamine (Mast Cells) Seratonin (Platelets)
- 81. Normal flow Stasis ACUTE INFLAMMATION HEMOCONCENTRATION AND STASIS
- 88. ACUTE INFLAMMATION PHAGOCYTOSIS - ATTACHMENT
- 89. ACUTE INFLAMMATION PHAGOCYTOSIS - ENGULFMENT
- 90. ACUTE INFLAMMATION PHAGOCYTOSIS – KILLING AND DEGRADATION
- 92. 2. Phagocyte Migration and Margination Margination is the process in which phagocytes stick to lining of blood vessels. Diapedesis (Emigration): Phagocytes squeeze between endothelial cells of blood vessels and enter surrounding tissue.
- 93. Phagocytes are attracted to site of infection through chemotaxis. Phagocytes destroy microbes, as well as dead and damaged host cells. 3. Tissue Repair Dead and damaged cells are replaced.
- 101. ACUTE INFLAMMATION SUPPURATIVE / PURULENT
- 102. ACUTE INFLAMMATION SUPPURATIVE / PURULENT - ABSCESS
- 103. ACUTE INFLAMMATION SUPPURATIVE / PURULENT - ABSCESS
- 104. ACUTE INFLAMMATION SUPPURATIVE / PURULENT - EMPYEMA
- 105. Thomas McGovern M.D. ACUTE INFLAMMATION ULCERATIVE
- 108. Atlanta South Gastroenterology, P.C. ACUTE INFLAMMATION PSEUDOMEMBRANOUS
- 109. Antimicrobial Substances: I. Complement System: Large group of serum proteins that participate in the lysis of foreign cells, inflammation, and phagocytosis.
- 110. II. Interferons: Antiviral proteins that interfere with viral multiplication. • Small proteins (15,000 to 30,000 kDa) • Heat stable and resistant to low pH • Important in acute and short term infections. • Have no effect on infected cells. • Host specific, but not virus specific.
- 111. Interferon alpha and beta: Produced by virus infected cells and diffuse to neighboring cells. Cause uninfected cells to produce antiviral proteins (AVPs). Interferon gamma: Produced by lymphocytes. Causes neutrophils to kill bacteria.
- 112. Two mechanisms of complement activation:
- 113. 1. Classical Pathway: Initiated by an immune reaction of antibodies. 2. Alternative Pathway: Initiated by direct interaction of complement proteins with microbial polysaccharides. Both pathways cleave a complement protein called C3, which triggers a series of events.
- 114. Classical Complement Pathway is Triggered by Antibodies Binding to Foreign Cells
- 115. Both Classical and Alternative Complement Pathways Trigger the Cleavage of C3
- 117. 1. Cytolysis: Due to the formation of a membrane attack complex (MAC) which produces lesions in microbial membranes. 2. Inflammation: Complement components (C3a) trigger the release of histamine, which increases vascular permeability.
- 118. 3. Opsonization: Complement components (C3b) bind to microbial surface and promote phagocytosis. 4. Inactivation of Complement: Regulatory proteins limit damage to host cells that may be caused by complement.
- 119. Classical and Alternative Complement Pathways Cause Inflammation, Opsonization, and Cytolysis
- 120. Cytolysis Caused by Membrane Attack Complex
- 121. Thank you…