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Immunology > 2.1 Principles of innate immunity to infection > Flashcards

2.1 Principles of innate immunity to infection Flashcards

1
Q

Protection of epithelial surfaces (8)

A
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2
Q

Physical & biochemical barriers: Skin

A

SKIN:
– Thick layer of cells
– Sebaceous gland secretions
- on surface contain fatty acids

PROBLEMS: pathogens can get into tissue via
– Wounds
– Vector-borne pathogens
(e.g. Lyme disease spread by ticks)

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3
Q

Physical & biochemical barriers: mucous membranes

A

MUCOUS MEMBRANES:
- Mucociliary escalator, peristalsis
- Coughing and sneezing / Vomiting and diarrhoea

Secretions (saliva, tears and mucous)
• Physical properties (washes away organisms)
• Anti-microbial properties (e.g. lysozyme)

Commensal microflora

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4
Q

commensal bacterial flora (microbiome) :

A
  • is an important defence for mucosal surfaces
  • contain friendly bacteria that will die via acid in stomach
    Ex: milk
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5
Q

provides the ‘early warning system’ for infection?

A

Innate immunity

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6
Q

Innate immunity used ___ to detect microbial components that are intrinsically foreign?

A

Pattern recognition receptors (PRR)

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7
Q

Innate immunity: PAMPs (3)

A

– Lipopolysaccharide
– Peptidoglycans
– Mannose

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8
Q

Bacteria PAMPs:
- Gram positive
- Gram negative

A
  • Gram positive = peptidoglycan
  • Gram negative = lipopolysaccharides
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9
Q

Receptors associated with membrane ?

A

Toll- like reaceptors

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10
Q

Receptor associated with cytoplasm?

A

NOD receptors

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11
Q

Recognize gram positive bacteria?

A

TLR-2

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12
Q

Recognize gram negative bacteria?

A

TLR-4

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13
Q

Recognize virus nuclei acid?

A

TLR-3 and TLR-5

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14
Q

What do viruses not have?

A

Structural PAMPs

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15
Q

How are viruses detected?

A

Viruses are detected by the presence of dsRNA produced during replication (not found in mammalian cells)

  • cells respond by producing interferons
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16
Q

Functions of type 1 interferons:

A

Resistance to viral replication
– Increased degradation of viral mRNA
– Increased antigen presentation of viral antigens
– Inhibition of viral protein synthesis

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17
Q

Infected cell signaling:

A

-signals neighboring uninflected cells to destroy RNA and reduce protein synthesis
- Signals neighboring INFECTED cells to undergo apoptosis
- activates immune cells

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18
Q

What type of cells can viruses infect?

A

Any nuclear cell

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19
Q

All nucleated cells can respond to viral infection by producing ____?

A

Type 1 interferons

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20
Q

What is interferon omega used to treat?

A

Persistent viral infection in cats
Ex: FeLV / FIV - won’t cure it but will reduce viral application and burden

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21
Q

Natural killer cells (NK) recognize?

A

Recognise decreased levels of MHC molecules on host cells
Recognize a symptom of viral infection

– decreased production during viral protein synthesis
– some viruses block transport to cell surface

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22
Q

NK Cell process:

A
  1. NK cells monitor cell surface expression of MHC molecules
  2. NK cells leave healthy cells alone
  3. in an infected cell, MHC production can be blocked by the virus, this activated NK cell to release cytotoxic granules
  4. Which kills the infected cell before viral replication is complete
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23
Q

___ is relatively weak to viruses?

A

Innate immunity

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24
Q

___ is a natural antiviral?

A

Interferon
- slows viral replication
- makes cells more resistant to infection

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25
Q

___ are able to identify and kill some infected cells (not efficient)

A

NK cells

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26
Q

_____ keeps you alive till adaptive immunity develops

A

Innate immunityq

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27
Q

Innate immunity to bacteria

A

Cellular mechanisms
– Recognition of pathogen
(membrane, vesicular and cytoplasmic PRRs)
– Response: Phagocytosis & inflammation

Humoral mechanisms
– Recognition of pathogen (soluble PRRs)
– Response: Killing of foreign organism,
Enhanced phagocytosis, Inflammation

28
Q

TTLR-2 recognize

A

Peptidoglycan

29
Q

TLR-4 recognize

A

Lipopolysaccharides

30
Q

TLR-5 recognize

A

Flagellin

31
Q

TLR- 9 recognize

A

Prokaryotic DNA

32
Q

NOD2 recognize

A

Muramyl dipeptide:
- degradation product of peptidoglycan
- present in cytoplasm of wbc

33
Q

A defect in the NOD2 receptor is responsible for

A
  • Crohn’s disease in humans
  • possibly IBD or anal furunculosis
34
Q

Recognition of bacteria by macrophage TLRs leads to

A

Phagocytosis and an inflammatory response

35
Q

What performs phagocytosis?

A

Neutrophils and macrophages

36
Q

___ are endocytosed, killed, and digested

A

Bacteria

37
Q

Good way to get rid of bacteria ?

A

Phagocytosis

38
Q

Respiratory burst:

A
  • enhanced cellular aerobic metabolism
  • reactive oxygen intermediates (ROI) are produced
  • The oxygen-dependent mechanism of bacterial killing
39
Q

are cytoplasmic organelles containing defensins, lactoferrin and acid proteases?

A

Lysosomes - fuse with phagosome, releasing their contents

40
Q

Lysosomes: defensins

A

Cationic anti-microbial peptides that damage bacterial cell walls

41
Q

Lysosomes: lactoferrin

A

– Binds and chelates free iron, which is required for bacterial growth/replication

42
Q

Lysosomes: acid proteases

A

Digestive enzymes active at a low pH

43
Q

The phago-lysosome becomes increasingly acidic as __ ions are pumped in.

A

H+ : The acidic environment activates the acid protease enzymes and the micro-organism is digested.

44
Q

inflammatory mediators:

A
  • histamine
  • pro-inflammatory cytokines
  • Lipid mediators of inflammation
45
Q

Histamine is produced by

A

Mast cells in degranulation in tissues

46
Q

Pro-inflammatory cytokines are synthesized by

A

predominantly by white blood cells and macrophages
– e.g. Tumour necrosis factor alpha (TNF-α)

47
Q

Lipid mediators of inflammation are derived from

A

arachidonic acid by actions of cyclooxygenases (COX) and lipoxygenases
– e.g. prostaglandins and leukotrienes

48
Q

Inflammatory cytokines: Localised effects

A

Vasodilation
– Increased blood flow to tissues (increased heat and redness)

Increased capillary permeability
– increased fluid leakage into tissues - Oedema (increased tissue swelling)

Influx of white blood cells
– Migration of phagocytic cells into tissues

49
Q

Systemic effects of inflammatory cytokines:
- Hypothalamus
- Liver
- bone marrow

A

Hypothalamus
– Fever

Liver
– Acute phase response

Bone marrow
– Neutrophil and monocyte mobilization

50
Q

Humoral (liquid) mechanism of innate immunity

A
  • acute phase proteins
  • complement cascade
51
Q

Acute phase response

A

Acute phase proteins stick to bacterial cell walls and enhance phagocytosis

52
Q

Where are complement proteins found?

A

In the blood

53
Q

Complement system:

A
  • Series of enzyme activation steps forming an amplification cascade
  • small amount of activation is amplified to generate large response
    **similar to clotting cascade, but different outcome
54
Q

Complement system diagram:

A
55
Q

Membrane attack complex ( MAC):

A
56
Q

is a vital component in the complement cascade

A

Complement protein C3

57
Q

Complement protein C3

A
  • C3 is a pro-enzyme
  • It is converted to C3a & C3b
58
Q

Where is C3b deposited?

A

On the bacterial surface:
– Acts as a marker for recognition by complement receptors on phagocytic cells
– Acts as an enzyme to facilitate the production of the Membrane Attack Complex

59
Q

C3a:

A

is released and stimulates an inflammatory response

60
Q

acts as a target for macrophages & neutrophils stimulating phagocytosis

A

C3b:

61
Q

acts as an enzyme to catalyse the formation of the MAC

A

C3b

62
Q

stimulates MAST CELL degranulation and triggers an inflammatory response

A

C3a

63
Q

Bacteria are attacked by __ and ___

A

cellular and humoral mechanisms of innate immunity

64
Q

___ and ___ eat, kill, and digest bacteria

A

Neutrophils and macrophages

65
Q

Inflammatory response helps to recruit?

A

Neutrophils and monocytes to the site of infection

66
Q

___ and ___ enhance phagocytosis and cause direct lysis

A

Circulating acute phase proteins and complement proteins

Immunology (10 decks)

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