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BIOL3003 > L24: Immunity bacteria and virus > Flashcards

L24: Immunity bacteria and virus Flashcards

1
Q

Barrier Breach (4)

A

Due to injury, acute inflammation, mobilisation of innate immune responses:

  1. Tissue damage causes release of vasoactive and chemotactic factors that trigger a local increase in blood flow and capillary permeability
  2. Permeable capillaries allow an influx of fluid (exudate) and cells
  3. Phagocytes migrate to site of inflammation (chemotaxis)
  4. Phagocytes and antibacterial exudate destroy bacteria
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2
Q

Types of inflammation (2)

A
  1. Acute: caused by tissue injury and invading microorganisms
  2. Chronic: autoimmune/auto-inflammatory diseases e.g. RA, inflammatory bowel disease, chronic infection
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3
Q

Inflammation vs immunity (3)

A
  1. Inflammation is nonspecific
  2. Immunity is antigen-specific and demonstrates memory
  3. With inflammation, a secondary exposure to a stimulus will demonstrate the same response as the initial incident
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4
Q

Challenges faced by immune system before antigen-specific adaptive immunity kicks in

A
  1. Diversity of microbial species seeking to invade
  2. Ongoing diversification within a given species of pathogen, much faster than the host can evolve new immune elements (e.g. spontaneous mutation, immune-pressure-driven selection, acquisition of pathogenicity islands via plasmids)
  3. Disparity of replication times: much faster for microbes than for host cells
  4. Nonselectivity of lethal chemical reactions: How to kill a microbe but spare a host cell containing the microbe or situated next to it
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5
Q

Innate immunity: soluble factors (SF) - acute phase proteins

A
  1. Both CRP and MBL active complement

2. Serum levels of C-reactive protein (CRP) used as an indicator of inflammation

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6
Q

Innate immunity: soluble factors (SF) - complement system; pathways and initiators (3)

A
  1. Classical: immune complexes, apoptotic cells, certain viruses and gram-negative bacteria, c-reactive protein bound to ligand
  2. Mannose-binding lectin: microbes with terminal mannose groups
  3. Alternative: many bacteria, fungi, viruses, tumour cells
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7
Q

C3a/C3b/C5

A

C3a: high chemotactic potential
C3b: deposited on surface of target cells forming C5 convertase.
C5: cleaved to produce C5a and C5b (beginning of membrane attack complex)

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8
Q

Neutrophils (PMNs)

A

Main line of defence against invading bacteria, primary function is phagocytosis and killing of pathogens. Directed during infection:

  1. Extravasation: cross the capillary wall from bloodstream closest to site of infection
  2. Chemotaxis: migrate towards source of infection through local tissues
  3. Recognise and phagocytose the invading organism
  4. Kill the organism
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9
Q

Phagocytosis steps

A
  1. Bacterium becomes attached to membrane evaginations called pseudopodia
  2. Bacterium is ingested, forming phagosome
  3. Phagosome fuses with lysosome
  4. Lysosomal enzymes digest captured material
  5. Digestion products are released from cell
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10
Q

Reactive Oxygen Intermediates (ROI)

A

Second line of antimicrobial products: oxidative burst and myeloperoxidase
oxygen - superoxide anion - hydrogen peroxide - hypohalous acids

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11
Q

Macrophages

A
  1. Endocytosis, phagocytosis and clearance of microorganisms, dead and dying cells, toxins and waste
  2. Antigen processing and presentation
  3. Wound repair, tissue homeostasis
  4. Protection against tumours; propagation of metastasis
  5. Regulation of Haematopoiesis
  6. Regulation of extracellular matrix composition
  7. Regulation of lipid and iron metabolism
  8. Regulation of coagulation and fibrinolysis
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12
Q

Mediators of radical-independent killing in the phago-lysosome; effector molecule and function (4)

A
  1. Cationic proteins (cathespin): damage to micorbial membranes
  2. Lysozyme: hydrolyses mucopeptides in the cell wall
  3. Lactoferrin: deprives pathogens of iron
  4. Hydrolytic enzymes (proteases): digests killed organisms
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13
Q

Consequences of macrophage activation

A
  1. Induction of antimicrobial mechanisms
  2. Induction of costimulatory molecules for T cells
  3. Release of chemokines, cytokines and inflammatory lipid mediators
  4. Release of proteases and other hydrolases
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14
Q

Antibody responses (2)

A
  1. Major antigens of many bacteria are polysaccharides and defence is mediated only by antibodies; these T cell-independent antibody responses may be short-lived and weak: low-affinity, poor memory, few long-lived plasma cells, IgM>IgG
  2. Helper T cell-dependent antibody responses to protein antigens are more effective: high affinity; IgG, IgA>IgM; long half-life of IgG; long-lived plasma cells; good memory
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15
Q

Injurious effects of anti-bacterial immunity (4)

A
  1. Local: acute inflammation, tissue damage
  2. Systemic effects of inflammation: cytokine mediated
  3. Septic shock: shock, disseminated intravascular coagulation, metabolic abnormalities caused by cytokines
  4. Rare late sequelae: immune complex diseases, cross-reactive responses against self antigens
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16
Q

Roles of antibodies and CTLs in adaptive immunity to viruses (2)

A
  1. Antibodies neutralise viruses and prevent infection: blocks infectious virus early in course of infection (before entering cells) or after release from infected cells (prevents cell-to-cell spread)
  2. CTLs kill infected cells and eradicate reservoirs of established infection: in some latent viral infections, CTLs control but do not eradicate the infection; defective T cell immunity leads to reactivation of the virus
17
Q

Immune evasion by viruses (2)

A
  1. Antigen drift, antigen shift: influenza, HIV, rhinovirus
  2. Inhibition of the class 1 MHC antigen processing pathway: different viruses use different mechanisms, NK cells are the host adaptation for killing class 1 MHC-negative infected cells
18
Q

Inhibition of MHC Class 1 pathway of antigen processing (5)

A
  1. Inhibition of proteasomal activity
  2. Block in MHC synthesis or ER retention
  3. Block in TAP transport
  4. Removal of Class 1 from ER
  5. Interference with CTL recognition by decoy viral class 1 like molecules

BIOL3003 (26 decks)

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