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POM CELLS > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What are the four cardinal features of inflammation?

A

Rubor - redness
Calor - heat
Tumor - swelling
Dolor - pain

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2
Q

What causes rubor?

A

Vascular leakage leads to an accumulation of blood contents, including red blood cells which causes the redness

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3
Q

What causes calor at a site of inflammation?

A

High metabolism of infiltrating immune cells all generate heat. Also the increased presence of fluid at core body temperature at a site that usually has limited exposure

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4
Q

What is inflammation?

A

A non specific immune response to cellular injury which is designed to remove damaged cells and clear threats such as infections and pathogens

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5
Q

What are the causes of inflammation?

A

Pathogens, allergens, physical damage, extreme temperatures, autoantigens

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6
Q

Where can inflammation occur?

A

Any vascularised tissue

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7
Q

When is inflammation initiated?

A

When cellular damage leads to the release of Damage Associated Molecular Pathogens (DAMPs) or Pathogen Associated Molecular Pathogens (PAMPs)

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8
Q

What causes swelling at a site of inflammation?

A

Vascular leakage increases blood flow into the inflamed tissue, leading to tissue buildup

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9
Q

What causes pain in an inflamed area?

A

Many of the mediators (e.g. prostaglandins) that signal to endothelial and immune cells during inflammation also signal on local nerve cells

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10
Q

What is meant by acute inflammation?

A

A short term process occuring in response to tissue injury, normally associated with rapid onset and resolution

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11
Q

What is acute inflammation characterised by?

A

Neutrophil recruitment

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12
Q

What triggers the release of DAMPs and PAMPs?

A

Non-apoptotic cell death eg due to a wound for example

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13
Q

What vasodilators do mast cells release?

A

Nitric oxide and histamine

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14
Q

What are the vascular changes associated with the release of histamine and nitric oxide?

A
  • Increase permeability of blood vessel wall
  • Dilation
  • Plasma leakage
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15
Q

What 4 benefits does increased vascular permeability and leakage into an inflamed site bring?

A

BALP

forms a BARRIER
more ANTIBODIES
more LEUKOCYTE migration
more PROTEINS to the site

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16
Q

How do neutrophils move to areas of damage?

A

Via chemotaxis, following a concentration gradient of chemotoxins including C5a, LTB4 and bacterial peptides

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17
Q

What is exudate?

A

Fluid, protein and cells that have seeped out a blood vessel

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18
Q

What does the exudate form?

A

A separation between healthy tissue and the inflamed tissue - acts as a physical barrier

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19
Q

How are neutrophils able to migrate towards the chemokine source?

A

They express complementary chemokine receptors which allow them to migrate towards the course

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20
Q

What is meant by neutrophil extravasation?

A

The movement of neutrophils from the vasculature into the surrounding tissue to reach the site of inflammation

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21
Q

What are the four steps of neutrophil extravasation?

A
  1. Chemo-attraction
  2. Rolling adhesion
  3. Tight Adhesion
  4. Transmigration
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22
Q

What are the two adhesion molecules which are upregulated by cytokines?

A

P-selectin and E-selectin

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23
Q

How do neutrophils recognise selectin molecules on the endothelium?

A

They have complementary carbohydrate ligands which bind to the selectin molecules

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24
Q

What is rolling adhesion?

A

When there is gentle interaction between the selectin molecules and the surface ligands which bind, causing the neutrophils to roll along the endothelium

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25
Q

What is the name of the P selectin ligand?

A

PSGL1

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26
Q

What promotes the low to high affinity switch in integrins?

A

Chemokines

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27
Q

What is meant by transmigration?

A

The movement of the neutrophil through the endothelial wall which involves the cytoskeleton of the neutrophil to be rearranged

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28
Q

What molecule mediates the transmigration of the neutrophil molecule?

A

PECAM

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29
Q

What are the three functions of neutrophils at the site of inflammation?

A
  1. Pathogen recognition
  2. Pathogen clearance
  3. Cytokine secretion
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30
Q

How do neutrophils recognise pathogens?

A

They use the TLR4 receptor to identify lipopolysaccharides that are present in gram negative bacteria for example

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31
Q

How do neutrophils clear pathogens?

A

By phagocytosis

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32
Q

Describe the process of phagocytosis?

A
  1. Pathogen is engulfed into phagosome
  2. Phagosome fuses with enzyme containing vesicles forming a phagolysosome
  3. This is degraded by enzymes through acidifcation
33
Q

What is released during phagocytosis which causes oxidative damage?

A

ROS - reactive oxygen species

34
Q

Give 3 reasons why the release of exudate is helpful?

A

Leads to increased lymphatic drainage and also allows plasma proteins like fibrin to be directly delivered to site of inflammation. Also helps to form a physical barrier between inflamed and healthy tissue

35
Q

Why are histamine molecules turned over rapidly?

A

They are small molecules and therefore are rapidly degraded

36
Q

What produces anti-inflammatory mediators to resolve acute inflammation?

A

Macrophages

37
Q

How can acute inflammation be resolved through repair?

A

Infiltrating WBC clear the wound of dead cells and pathogens and release growth factors which stimulate tissue repair - ECM deposition

38
Q

How do macrophages clear apoptotic cells?

A

They engulf them

39
Q

When does chronic inflammation occur?

A

When the acute response cannot clear the stimuli

40
Q

What does chronic inflammation result in?

A

Scarring and loss of tissue function

41
Q

What drives continual inflammation in chronic inflammation?

A

Antigens

42
Q

Why is persistent neutrophil activation bad?

A

It is highly toxic and leads to rapid tissue destruction

43
Q

What is a foreign antigen?

A

an antigen derived from molecules not found in the body

44
Q

What is a self antigen?

A

An antigen derived from molecules produced by our bodies

45
Q

What is an immunogen?

A

An antigen independantly capable of driving an immune response in absence to additional substances

46
Q

What is a hapten?

A

A small molecule that alone does not act as an antigen but when bound to a larger molecule it can create an antigen

47
Q

What is granulomatous inflammation?

A

Chronic inflammation with distinct patterns of granuloma formation

48
Q

Name some diseases characterised by chronic inflammation?

A

Rhuematoid Arthritis
Asthma
Inflammatory Bowel Disease
Hepatitis
Psoriasis

49
Q

Name some diseases associated with granulomatous inflammation?

A

TB
Leprosy
Tumour reactions
Crohn’s Disease

50
Q

What are some persistent inflammatory stimuli found in chronic inflammation?

A

Persistent/prolonger infection

Persistent toxic stimuli like allergens and pollutants

Unclearable particulates

Self-antigens

51
Q

What does the distinct immune cell infiltrate found in chronic inflammation consist of?

A

Inflammatory macrophages
T cells
Plasma Cells

52
Q

How are macrophages recruited to the site of inflammation?

A

As monocytes

53
Q

What are the benefits of macrophages being recruited to the site of inflammation?

A

Phagocytosis
Cytotoxic
Anti-inflammatory
Help repair wound by building ECM

54
Q

What are the bad things associated with macrophages being recruited to the area?

A

They can cause damage to healthy surrounding tissue
Inflammatory
Pro-fibrotic, deposit excess collagen

55
Q

What pro-inflammatory signals do T cells release?

A

TNF, IL-17 and IFN-gamma

56
Q

How do T cells promote remodelling and suppression of the immune system?

A

TGF-beta

57
Q

How do T cells act in a cytotoxic manner?

A

through the release of perforin and granzymes

58
Q

What do B cells do in an chronic inflammatory response?

A

Generate antibodies that help to clear infection

59
Q

Which white blood cell can act remotely during chronic inflammation?

A

B cells

60
Q

What are granulomas?

A

Aggregation of activated macrophages

61
Q

What triggers granuloma formation?

A

Strong T cell responses

62
Q

What is the job of the granulomas?

A

To form a physical barrier to prevent pathogenic material from leaking out granuloma, thus allowing macrophages to clear the material

63
Q

What are the differences between acute and chronic inflammation?

A

Acute:
- Rapid onset
- Lasts days
- Vasodilation
- Neutrophils predominate
- Histamine release
- Scarring
- Either resolved or moves on to chronic inflammation

Chronic:
- Delayed onset
- Lasts years
- Ongoing tissue injury and attempts at healing
- Monocytes and macrophages dominate
- Prominent scarring

64
Q

What type of cell dominates during chronic inflammation?

A

Monocytes / Macrophages

65
Q

How long may a chronic inflammatory reaction last for?

A

Weeks, months or even years

66
Q

What is continually released during chronic inflammation?

A

Cytokine release

67
Q

What are the long term consequences of inflammation called?

A

The sequelae

68
Q

What are the three possible outcomes of injury?

A
  1. Regeneration
  2. Repair / scar formation
  3. Tissue scarring categorized by chronic inflammation
69
Q

What does resolution after injury involve?

A

The clearance of injurious stimuli, and inflammatory mediators, replace injured cells and return to normal function

70
Q

What does fibrosis involve as an sequalae of inflammation?

A

the deposition of collagen leading to excess tissue scarring and therefore the inability of the tissue to carry out its function

71
Q

What is deposited when wounds heal?

A

ECM deposited

72
Q

How do scars form?

A

When the collagen is unable to be removed from the site of endothelial repair

73
Q

What are the positive outcomes of inflammation?

A

Clear inflammatory agent.
Remove damaged cells
Restore normal tissue function

74
Q

What are the negative outcomes of inflammation?

A

Excess tissue damage
Scarring
Loss of organ function -> organ failure

75
Q

What does a histopathologist do?

A

Deals with tissues, examines them and notes the architecture of the tissue and identify what it tells us about a particular condition

76
Q

Describe how neutrophils are able to emigrate through the blood vessel walls?

A

Through the relaxation of inter-endothelial cell junctions and digestion of vascular basement membrane

77
Q

Which chemokines released by macrophages cause chemo-attraction of neutrophils to the site of injury?

A

TNF and IL-1

78
Q

Which chemokines cause the switch from low affinity ligands to high affinity ligands?

A

LFA-1 and MAC-1

POM CELLS (15 decks)

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