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Immunology and Microbiology

Immunology and Microbiology. Host-Microbe Interactions. Non-specific (Innate) Immunity. First line of defense (Non-specific resistance) Physical and Chemical Defenses Normal Flora Second line of defense (Non-specific resistance) Phagocytosis Inflammation Fever

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Immunology and Microbiology

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  1. Immunology and Microbiology

  2. Host-Microbe Interactions Non-specific (Innate) Immunity

  3. First line of defense (Non-specific resistance) • Physical and Chemical Defenses • Normal Flora Second line of defense (Non-specific resistance) • Phagocytosis • Inflammation • Fever • Antimicrobial substances: Complement, Interferon Third line of defense (Specific Resistance) • Antibodies • B cells and T cells

  4. Detect enemy Immobilize/kill enemy Send out alarm Recruit help Make environment unpalatable for enemy/prevent spread (process repeats) Toll-like receptors on macrophages; complement (3 ways) Phagocytosis; lysis Cytokine release Inflammation; fever

  5. Toll-like receptors: What are some evolutionarily conserved features of microbes that our immune cells could recognize? Step 2.

  6. Steps in phagocytosis http://www.cellsalive.com/mac.htm

  7. Clinical and laboratory features of patients with an inherited deficiency of neutrophil membranecomplement receptor type 3 (CR3) and the related membrane antigens LFA-1 and p150,95. Ross GD. Over the last 3 years a group of more than 20 patients has been described worldwide who have a similar history of recurrent bacterial infections and an inherited deficiency of three related leukocyte membrane surface antigens known as CR3, LFA-1 and p150,95 (function unknown). It is believed that the patients with this disease have a reduced or absent expression of all three antigen family members on different WBC types. Neutrophils have a reduced phagocytic response to bacteria and yeast as well as a reduced ability to migrate into sites of infection. • Adapted from J Clin Immunol. 1986 Mar;6(2):107-13.

  8. The Complement System • Activated in 3 ways • Antibody-antigen (augments specific defense) • Molecules that recognize bacterial sugar polymer (mannan) • “Random binding” to cell surfaces (C3b) • Triggers a cascade • 3 effects

  9. Effects of complement system 1. Opsonization

  10. 2. Membrane Attack Complex (Lysis) Are G+ or G-ve cells more susceptible to killing by MAC? Why?

  11. Bacterial cell wall structure Gram-negative and gram-positive bacteria http://www.blackwellpublishing.com/trun/artwork/Animations/Overview/overview.html

  12. 3. Inflammation • What else triggers inflammation? Tissue damage • What are features of inflammation? • What is the inflammatory process?

  13. Which of the following statements about inflammation is false? • Vasodilation results in leakage of blood components • The process can cause damage to host tissue • It is always accompanied by a fever • The signs of inflammation are redness, swelling, heat and pain • It can be triggered by activating toll-like receptors (macrophages produce cytokines)

  14. INFLAMMATORY PROCESS trauma or infection vasodilation chemotaxis and diapedesis

  15. Is that pus? Is inflammation a good thing?

  16. The movement of phagocytes in the direction of an infection, due to attraction by complement, chemicals released by microorganisms, and the remnants of damaged cell membranes is a process called A) phagocytosis. B) chemotaxis. C) diapedesis. D) cytoadherence.

  17. Hypothalamus controls body temp Pyrogens resets temp set point Pyrogens: cytokines; LPS Unfavourable for bacterial replication Favourable for immune response--phagocytosis; lymphocyte replication etc FEVER

  18. Interferon and viral infections: a protective alerting system

  19. Complement and immunoglobulins can coat the outer surface of a microorganism, enhancing phagocytosis. This process is called A) chemotaxis. B) fixation. C) opsonization. D) endotoxicity. E) membrane attack complexing.

  20. Host-Microbe Interactions1. Innate (Non-specific) Defenses a. Chemical and Physical; (Biological) b. Normal Flora

  21. Host-Microbe Interactions 1. Contact with microbe a. colonization (normal flora) b. defense breached c. Loss d. Allergy 2. Infection a. cure, immunity b. establishment c. carrier 3. Disease

  22. All of the following statements are true with regard innate immunity EXCEPT: A)These responses are not directed specifically to the infectious agent. B)These responses are not affected by prior exposure to the agent. C)These responses are inborn. D)These responses are operating constantly to prevent the establishment of any infection. E)All of the above are true with regard to innate immunity.

  23. First line of defense BarriersPhysical Chemical

  24. An enzyme found in our tears, saliva, serum, and mucus that degrades the peptidoglycan of the cell wall of Gram-positive bacteria is called A) amylase B) lysozyme. C) keratinase. D) streptokinase. E) peptidase.

  25. First line of defense-Chemical & Physical Barriers

  26. Which of the following substances is produced by the cells in our body and interferes with the multiplication of viruses by stimulating the production of antiviral proteins? A) antivirase. B) interferon. C) inhibitase. D) complement. E) multiplicase.

  27. Which of the following are mechanisms that protect the respiratory system from infection? 1. mucus 2. mucociliary escalator 3. normal flora 4. lysozyme 5. acidic environment A)1,2,5. B)1,3. C)1,2,3. D)2,4. E)1,2,3,4.

  28. Normal Flora of Humans

  29. What normal flora? • A normal human has approximately 1013 body cells and 1014 individual normal flora! • microbes that grow on external and internal surfaces of the body without producing obvious harmful effects • Transient microbial flora : only occasionally inhabit the body. • Symbiotic relationships: Commensal, Mutualistic, Parasitic

  30. Body sites that harbor normal flora

  31. Importance of the normal flora • Prevent attachment of invading organisms • Produce antimicrobial substances against other microbes that are pathogens • Stimulate immune system • Cause the production of cross-reacting antibodies • Significant nutritional source of vitamins • Cause dental caries and gum disease

  32. How do we acquire microflora? • During birth & within first 12 hours after delivery • Breast-fed v bottle-fed • Contact with people, environment, food. • Eruption of teeth & introduction of solid food.

  33. What leads to changes in the normal flora? • Antibiotic treatment • Immunosuppression • Diet • Changes in physiology , e.g. estrogen-glycogen effect

  34. Normal Skin Flora • 1000 to >1 million/ cm2 • Diphtheroids: G+ rods & cocci, e.g. Corynebacterium & Proprionobacterium , e.g. P.acnes (acne) • facultatively anaerobic, coagulase negative Staphylococci [carriers of coagulase positive S. aureus in population] • Yeasts

  35. First line of defense (Non-specific resistance) • Physical and Chemical Defenses • Normal Flora • Second line of defense (Non-specific resistance) • Phagocytosis • Inflammation • Fever • Antimicrobial substances: Complement, Interferon • Third line of defense (Specific Resistance) • B cells and T cells • Antibodies and Humoral Response • Cellular Mediated Immunity

  36. Genetic Immunodeficiencies Common Variable Hypogammaglobulinemia: Affecting both males and females and occurring at any age, this disease is manifest by repeated pyrogenic infections. The B cells fail to mature to plasma cells. Passive Ig is the common treatment. Chronic Candidiasis: Fungal infection by nonpathogenic yeast is the manifestation of a number of afflictions where few mature T cells are present. These patients often have B cells that respond to T-independent antigens, but Candida albicans (yeast) stimulates a poor antibody response. • What immune component fails to be made in CVH? • How come a defect in T cells affects antibody response in chronic candidiasis?

  37. The two arms of the adaptive immune system

  38. Antigen: a molecule (or parts of one) that causes antibody generation (Immunoglobulin) The specific region on an antigen recognized by an antibody

  39. Antibody Structure Diversity in antibodies due to variable region An infinitely large number of possible immunoglobulins; 5 different classes: IgG, IgM, IgA, IgD & IgE Made by V(D)J recombination http://en.wikipedia.org/wiki/V%28D%29J_recombination

  40. Effects of Antigen-Antibody Interactions Fig. 16.06

  41. Effects of Antigen-Antibody Interactions-2 Parasites; virally – infected host cells NK cells release perforins and proteases (16.8)

  42. How is the antibody response triggered? 1. T-cell dependent antigens 2. T-cell independent Ags e.g. polysaccharides, LPS response of young children to these antigens is poor Result: Clonal selection and expansion of B-cells

  43. Result: Memory A plasma cell Clonal Expansion • Negative selection • Affinity maturation • Class switching: IgM – IgG—IgG / IgA • Formation of memory cells Why is the RER in plasma cells so extensive?

  44. Memory Cells mediate secondary response and lifelong immunity Fig. 16.11

  45. Cellular Immunity • Cytotoxic T cells (CD8+) • Eliminates cells infected with virus, intracellular parasite • Helper T cells (CD4+) • Mediates B-cell proliferation; macrophage activation Both stimulated by dendritic cells (cells of innate immunity) Both produce cytokines that stimulate own proliferation

  46. T cells activated by dendritic cells A B C

  47. A. Recognition of virally-infected cell by cytotoxic T cell results in apoptosis

  48. B: Helper T-cell activation and interaction with B-cells

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