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Semester 1 (YEAR 2) - Lecture Notes > Week 2 - Bacterial cells, Immunity and Vaccines > Flashcards

Week 2 - Bacterial cells, Immunity and Vaccines Flashcards

1
Q

How does bacterial cells cause disease?

A
  1. Secretion systems
  2. Capsules
  3. Toxins
  4. Fimbria / pilli
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2
Q

How does secretion systems aid causation of disease?

A
  • export / inject effector protein across bacterial cell wall into host cell
    - proteins remodel cell cytoskeleton, promote host cell invasion + promote attachment to host cell
  • e.g. can inject own receptors into host for attachment of effector protein
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3
Q

How does fimbria / pilli aid causation of disease?

A

Found on outer membrane of bacterium
Allows bacterium to stick (adhesion) host cells
Aids biofilm formation + bacterium cell movement (twitching)

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4
Q

How does capsules aid causation of disease?

A
  • Protects cell from phagocytosis / the immune system
    - have surface charge (-ive) = can’t be engulfed by phagocytes
    - mimic host cells (non-immunogenic) = no alert to immune system
  • Allows immune evasion (= important for invasive infections)
    - causes host cell damage
  • Can be involved in attachment
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5
Q

How does toxins aid causation of disease?

A

Toxins damage systemic system

  1. Endotoxins
    - released when cell dies
    - part of gram -ive bacteria cell wall
    - low site speciality
  2. Exotoxins
    - produced by bacterial cell
    - high potency
    - high site specificity (= move through body to find specific target)
    - susceptible to temp.

3 Types:
1. Enzymatic - e.g. AB toxins help get enzyme into cell (A subunit ~ encodes catalytic activity, B subunit ~ binds to receptor+ translocation)
2. Pore forming - toxin attach to receptor in cell membrane + toxin experience conformational change = pore formed
- e.g. pneumolysin in CAP
3. Superantigens - activate many T-cells causing cytokine release
- force binds T-cell receptors and molecules on antigen presenting cells

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6
Q

How does pneumolysin (in CAP) aid causation of disease?

A

Inhibits mucociliary pathway
Cause macrophage death
Cause inflammatory mediated tissue disease (due to influx of neutrophils)

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7
Q

How are infections spread?

A

Airborne
Fomite (non-living)
Vertical (from parent to child)

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8
Q

What is innate immunity?

A

Ability to recognise + destroy pathogen / its product
- recognises pathogen-associated molecular patterns on pathogen
Doesn’t require previous exposure to pathogen
Microbiota (normal flora) - reduces risk of infection

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9
Q

What is adaptive immunity?

A

Acquired ability to recognise + destroy specific pathogen / its product
- recognises antigen (on pathogen)
Dependant on previous exposure to pathogen

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10
Q

What is natural immunity?

A

Natural active immunity - acquiring an infection which causes immune response

Natural passive immunity - antibody transfer through placenta / breast milk

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11
Q

What is artificial immunity?

A

Artificial active immunity - given controlled dose of antigen to induce production of antibodies (= vaccination)

Artificial passive immunity - injection of antiserum from an immune individual

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12
Q

How are antibodies produced?

A
  • First exposure to virus
  • WBC (B cells) recognises antigens (presented by pathogen) as foreign
  • WBC produces antibodies specific to antigen (clonal selection)
  • When B cell antibody binds to antigen = B cells divide = large increase in no. of B cells
  • Some B cells become plasma cells (which secrete antibodies)
  • Rest become memory cells

Antibodies are immunoglobulins (Ig)

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13
Q

How does vaccinations work?

A
  • Antigen is introduced into body causing immune system to attack the pathogen
  • Causes development of B memory cells (stored in lymph nodes)
  • Encounter same antigen again already have cells to destroy it (before disease develops)
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14
Q

What are the main types of vaccines?

A

Live attenuated -
- more effective

Non-viable / inactivated -

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15
Q

What is the UK immunisation schedule?

A
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16
Q

Why is the immune system important for human health?

A
  • Protects against pathogens e.g. virus, bacteria, fungi
  • Provides deference
  • Apoptosis / eliminates altered cells
17
Q

What are the mechanisms used by the immune system to defend against infection?

A
  1. Innate immune system
    (born with this)
    - first line defence
    - non specific (responds to all pathogens same way)
    - quick onset
  2. Adaptive immune system
    (develop as grow)
    - slow onset / activation
    - specific
    - produces memory cells
18
Q

Hematopoietic Stem Cell-derived Lineages and their use

A

H. stem cell differentiates to form other cells
Stem cells are from bone marrow

Common Lymphoid Progenitor:
- Lymphoid cells are used in adaptive system
- lymphoid stem cells produce B cells, T cells and natural killer cells

Myeloid Stem cells:
- produce CFU cells that produced neutrophils, monocytes (differentiate further into macrophages + dendritic cells), eosinophils, basophil, mast cells, megakaryocytes + erythrocytes

19
Q

Dendritic cells and their use

A
  • Are antigen presenting cells
  • Engulf antigen, break it down + present antigen on their weir cell surface
  • Dendritic cells activate T-cells, which produces B cells

(innate immune system)

20
Q

Macrophages and their use

A

-Are antigen presenting cells
- Engulf antigen, break it down + present antigen on their weir cell surface
- Activates T-cells, which produces B cells

(innate immune system)

21
Q

Neutrophils and their use

A
  • Migrate towards infection + engulf bacteria (small microorganism)
    - only bacteria as pathogen has to be smaller than cell
  • Phagocytosis of bacteria BUT DON’T present antigen on surface

(innate immune system)

22
Q

Basophil and their use

A
  • Involved in allergic reactions
  • Have receptors on surface that responds to antibodies

(innate immune system)

23
Q

Eosinophil and their use

A
  • Protect against parasites (large microorganism)
  • Breaks down parasite into smaller parts = can be engulfed by macrophages, dendritic cells or neutrophils

(innate immune system)

24
Q

Cytokines and their use and their use

A
  • Toxic to viruses

(innate immune system)

25
Q

Natural killer cells and their use

A
  • Destroy virus infected cells

(innate immune system)

26
Q

Mast cells and their use

A
  • Release factors which increase blood flow = attracts cells from immune system to site of infection

(innate immune system)

27
Q

Th / CD4+ cells and their use

A
  • Macrophages activate CD4+ cells
    - phagocytose / break down bacteria + present antigen on surface of Major Histocompatibility Complex (MHC)
  • CD4+ cells recognise antigens on Class II complex

Th (T helper cells):
Th1 = stimulates cell mediated immunity
Th2 = stimulate plasma cells + secretion of antibodies

(adaptive immune system)

28
Q

Tc / CD8+ cells and their use

A
  • Recognise antigens on Class I MHC

(adaptive immune system)

29
Q

B Lymphocytes and their use

A
  • Produce antibodies (immunoglobulin = Ig)
    -B cells are induced by diff. cytokines = differentiation in B cells produced = diff. antibodies produced

Immunoglobulin:
- prevents antigen binding to host cell + infecting it
- can bind to receptor on cells + attract other immune cells
-

(adaptive immune system)

30
Q

Hypersensitivity Reactions

A

Reaction that occurs in response to allergen e.g. pollen

Type 1:
- IgE mediated hypersensitivity
- allegers binds to receptor for IgE
- causes histamine production (i.e. sneezing, itching)

Type 2:
- IgG mediated cytotoxic hypersensitivy

Type 3:
- Immune complex mediated hypersensitivity
- causes aggregation of diff. immune complexes
- neutrophils recognise aggregation as infection = eliminate it

Type 4:
- Cell-mediated hypersensitivity
- Have proteins which activate T helper cells + produce cytokines which activate macrophages

31
Q

Allergies and therapeutic strategies

A

Allergies:
- Anti-histamine drugs = ease allergy symptoms
- bind to histamine receptor (preventing histamine from binding)

Drug Induced Allergies:
- Drug binds to receptor forming a complex
- Complex is recognised as foreign pathogen by APC
- immunes sits is activated = T cell activation

Semester 1 (YEAR 2) - Lecture Notes (6 decks)

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