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L2 Host Defences Flashcards

1
Q

What is disease?

A

The result of a host interaction with a pathogen (bacterial in this module)

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2
Q

Is disease a rare or common outcome of host-pathogen interaction?

A

Very rare

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3
Q

What 3 factors are taken into account for disease?

A

Host (human), pathogen (bacterium), environment/circumstances

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4
Q

Examples of ways the host can interact with the pathogen

A

Vectors (insects), food, sexually transmitted

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5
Q

If a pathogen affects a host, it is more virulent if…

A

it is transmitted to the host directly

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6
Q

What is responsible for 70-80% of infections?

A

Zoonosis

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7
Q

What must be overcome in order for disease to occur?

A

Host defences

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8
Q

What part of the immune system is responsible for non-specific defence mechanisms?

A

Innate

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9
Q

What part of the immune system is responsible for specific defence mechanisms?

A

Adaptive

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10
Q

What is the first line of the defence (innate)?

A

Constitutive - skin, mucous membrane, secretions of skin & mucous membrane

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11
Q

What is the second line of defence (innate)?

A

Inducible - phagocytosis, antimicrobial proteins, inflammatory response

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12
Q

What is the third line of defence (adaptive)?

A

Lymphocytes, antibodies

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13
Q

The innate immune system deals with __ infections.

A

acute

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14
Q

The adaptive immune system deals with…

A

reinfection

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15
Q

What are constitutive defences?

A
  • Provide general protection against invasion by normal flora, or colonisation/ infection/ infectious disease caused by pathogens
  • ‘Natural resistance’
  • Skin, mucosal surfaces, tears, saliva, sweat, urine, stomach acid etc.
  • Non-specific
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16
Q

What are inducible defences?

A
  • Must be induced by host exposure to a pathogen
  • Only triggered after host is appropriately exposed to pathogen
  • Immune responses
  • Usually specifically directed against an invading pathogen
  • Can be part of innate or acquired immune system e.g. cytokines, antibodies
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17
Q

What are components of non-specific defences?

A
  1. Anatomical defences
  2. Microbial antagonism
  3. Phagocytosis
  4. Tissue bactericides (incl. complement)
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18
Q

What is the largest organ?

A

The skin (surface area of 1.8 m²)

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19
Q

What are the conditions of the skin that bacteria do not like?

A
  • Dry
  • Acidic (pH 5.0)
  • Low temp.
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20
Q

Are resident microflora in the skin mainly Gram positive or negative?

A

Gram positive

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21
Q

What connects the skin to the immune system of the host?

A

SALT = skin associated lymphoid tissue

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22
Q

Where in the body would you find mucous membranes?

A

GIT, respiratory tract, urogenital tract

23
Q

What is the main function of epithelial cells?

A

Absorption of nutrients

24
Q

What are M cells?

A

Naturally phagocytic specialised epithelia that are continuously sampling the bacterial population in gut & transferring that info to immune cells

25
Why do many pathogens target M cells?
Because they know they will get across the gut barrier naturally
26
What epithelia is found mainly in the lungs & GIT?
Simple columnar epithelia
27
What facilitates the joining together of epithelial cells to form a barrier?
Tight junctions
28
What happens when pathogens target tight junctions?
Pathogen destabilises the tight junctions → get water & sometimes blood in the inside moving between cells and into the gut lumen. This causes bloody diarrhoea e.g. Clostridium perfringens
29
Where are M cells located?
In the follicle-associated epithelium, that covers Peyer's patches
30
M cells stimulate the production of which antibody?
sIgA
31
What do Goblet cells secrete?
Mucus
32
What do entero-endocrine cells secrete?
NA and other gut-localised hormones
33
What do Paneth cells secrete, and where do they stay localised?
Secrete antimicrobial peptides | Paneth cells stay localised in the crypt at the base of the villus
34
What are Defensins?
Antimicrobial peptides that form pores in bacterial membranes
35
What is another term for microbial antagonism?
Colonisation resistance
36
What is microbial antagonism?
Protection of the surfaces afforded by an intact normal flora (commensal flora) in a healthy host
37
Name 3 ways that the normal flora can protect mucosal surfaces
1. Competition for binding (colonisation) sites 2. Antagonism against non-indigenous species - highly specific proteins called bacteriocins produced by normal flora to kill/inhibit other species 3. Immunomodulation - normal flora interact with immune system to stop pathogen growth/survival
38
What are the first to arrive at a site of infection in response to chemokine signals produced in that locality?
Neutrophils, followed by monocytes which will develop into macrophages in tissue
39
What is neutropenia and what are sufferers very prone to?
Neutropenia is depressed polymorphonuclear leukocyte levels (low neutrophil levels) - sufferers very prone to infection
40
What is an example of a bacterium that lives in macrophages and hijacks the normal macrophage function?
Salmonella - uses macrophages as a privileged niche for its replication because they are a great source of nutrients
41
What are examples of tissue bactericides?
Transferrin Interferon Lysozyme antimicrobial molecule Complement
42
What is the role of transferrin?
Transferrin has a high affinity for iron, so it is released by the body during bacterial infection to reduce the iron available to invading bacterial cells. Its concentration increases during systemic infection.
43
What is the Red Queen Hypothesis?
Bacteria produce their own iron-binding molecules, called siderophores, that compete with the body for iron.
44
What does Interferon do?
It inhibits viral replication and activates other cells which kill pathogens
45
Where would you find lysozyme and what does it do?
Lysozyme is an antimicrobial molecule that is found in serum and tears. It breaks down the bacterial cell wall (peptidoglycan).
46
What is complement?
A set of serum (blood) proteins (C1-C9) which provide a form of constitutive defence
47
Where would you find complement, and what does it do?
In the blood. Serum proteins which cause destruction of microorganisms directly or with the help of phagocytic cells. Complement opsonises microorganisms, which makes them more susceptible to phagocytosis.
48
Briefly describe the complement cascade, that eventually leads to phagocytosis
- Ab binds bacteria in blood → activation of C1/2/4 complex → creates an active enzyme (C3 convertase) → cascade - C3 convertase cleaves C3 into 2 active subunits (C3a & C3b) - C3b binds bacterial cell wall → opsonisation - C3b also cleaves C5 into 2 subunits (C5a & C5b) - C5a attaches to macrophages & increases their activation - C3a & C5a attract & activate macrophages → engulf & destroy opsonised bacteria
49
What is the Classical Pathway?
When the complement cascade is triggered by an antibody
50
What is the Alternative Pathway?
If the body has never seen the bacteria before, complement can also function to attack that bacteria using the Alternative Pathway
51
What makes up the membrane attack complex (MAC), and what does it do?
MAC = C5b, 6, 7, 8, 9 | Forms pores in Gram negative cells
52
What immune functions does complement trigger?
- Phagocytosis - Inflammation - Membrane attack
53
Which complement protein has the most important opsonising activity?
C3b
54
What is the main aim of complement?
To keep the blood sterile and free of microorganisms

MB3001 (15 decks)

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