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POM Molecular Biology of the Cell > Inflammation > Flashcards

Inflammation Flashcards

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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
It is a complex and tightly regulated process

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5
Q

What are the causes of inflammation?

A

Pathogens, allergens, physical damage, extreme temperatures, auto-antigens, non-apoptotic cell death (necrosis and necroptosis)

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6
Q

What diseases can lead to inflammation?

A

Infection
autoimmunity
hypersensitivity
trauma
fibrotic disease
cancer

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7
Q

What cells are involved with inflammation?

A

epithelial and endothelial cells

Neutrophils
macrophages
lymphocytes
eosinophils
mast cells

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8
Q

Where can inflammation occur?

A

Any vascularised tissue

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9
Q

Is acute inflammation a fast or slow response?

A

Rapid response, non-specific response to cellular injury

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10
Q

What does acute inflammation lead to?

A

Change in local blood flow–>

Structural changes in the microvasculature–>

Recruitment/ accumulation of immune cells and proteins

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11
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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12
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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13
Q

What causes pain in an inflamed area?

A

Many of the mediators that signal to endothelial and immune cells during inflammation also signal on local nerve cells

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14
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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15
Q

What is acute inflammation characterised by?

A

Neutrophil recruitment

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16
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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17
Q

What vasodilators do mast cells release?

A

Nitric oxide and histamine

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18
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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19
Q

After damage to a steady state of an organ ie., the skin, what 3 things happen?

A
  1. inflammatory signals
    - non-apoptotic cell death
    - detection of foreign material
  2. vasodilators released
    - Histamine
    - Nitric oxide
  3. vascular changes
    - increased permeability
    - dilation
    - reduced flow
    - plasma leakage
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20
Q

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

A

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

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21
Q

What are soluble mediators released at injury?

A

Histamines, prostaglandins, cytokines (TNF, IL-1), Chemokines, Complement (C5a, C3a, C4a)

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22
Q

What are the principle sources and actions of histamines?

A

mast cells, basophils, platelets

vasodilation, increased vascular permeability, endothelial activation

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23
Q

What are the principle sources and actions of prostaglandins?

A

mast cells, leukocytes

vasodilation, pain, fever

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24
Q

What are the principle sources and actions of cytokines?

A

macrophages, endothelial cells, mast cells

endothelial activation (adhesion molecules), fever, malaise, pain, anorexia, shock

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25
Q

What are the principle sources and actions of chemokines?

A

leukocytes, activated macrophages

chemotaxis, leukocyte activation

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26
Q

What are the principle sources and actions of complement (C5a, C3a, C4a)?

A

Plasma (produced in the liver)

leukocyte chemotaxis and activation, vasodilation (mast cell stimulation), opsonisation

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27
Q

Why do we experience pain during inflammation?

A

Due to the release of prostaglandins

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28
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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29
Q

What is exudate?

A

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

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30
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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31
Q

What is immune cell recruitment?

A
  • recruitment and inflammation signals at the site of damage e.g., chemokines produced
  • chemokines diffuse out to form a gradient
  • leukocytes expressing complementary chemokine receptors migrate toward the chemokine source
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32
Q

What are examples of immune cell recruitment?

A

Chemokine: CXCL8 otherwise known as IL-8

Receptors: CXCR1 and CXCR2, g-coupled 7-transmembrane proteins

Cell type: Neutrophils. Often the first cell type recruited to the site of inflammation

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33
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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34
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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35
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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36
Q

What is chemo-attraction?

A

Cytokines-> endothelial
up-regulation of adhesion molecules
e.g., selectins

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37
Q

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

A

P-selectin and E-selectin

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38
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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39
Q

What is rolling adhesion?

A

carbohydrate ligands in a low affinity state on neutrophils bind to selectins
e.g., PSGL1 (selectin P ligand) binds P and E-selectins

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40
Q

What is the name of the P selectin ligand?

A

PSGL1

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41
Q

What is tight adhesion?

A

Chemokines promote low to high affinity switch to integrins LFA-1, Mac-1- enhance binding to ligands e.g., ICAM-1/2

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42
Q

What promotes the low to high affinity switch in integrins?

A

Chemokines

43
Q

What is meant by transmigration?

A

Cytoskeletal re-arrangement and extension of pseudopodia. Mediated by PECAM interactions on both cells.

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

44
Q

What molecule mediates the transmigration of the neutrophil molecule?

A

PECAM

45
Q

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

A
  1. Pathogen recognition
  2. Pathogen clearance
  3. Cytokine secretion
46
Q

How do neutrophils recognise pathogens?

A

They use the TLR4 receptor and CD14 to identify lipopolysaccharides (LPS) that are present in gram negative bacteria for example

47
Q

How do neutrophils clear pathogens?

A

By phagocytosis and netosis

48
Q

What does cytokine secretion lead to?

A

recruitment and activation of other immune cells

49
Q

Describe the process of phagocytosis?

A
  1. Pathogen is engulfed into phagosome
  2. Phagosome fuses with enzyme containing vesicles (lysosome) forming a phagolysosome
  3. This is degraded by enzymes through acidifcation
50
Q

What are some enzymes that could be in lysosomes?

A

elastase and lysozyme

51
Q

What is released during phagocytosis which causes oxidative damage?

A

ROS - reactive oxygen species
phagocyte NADPH oxidase
antimicrobial peptides e.g., defensins

52
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

53
Q

Why are histamine molecules turned over rapidly?

A

They are small molecules and therefore are rapidly degraded

54
Q

What are the 4 resolutions of acute inflammation in the resolution phase?

A
  1. pathogen recognition
  2. short half-life
  3. macrophages
  4. repair/ wound healing
55
Q

How does pathogen recognition occur?

A

Immune cells (e.g., neutrophils) and antimicrobials (e.g., antibodies) will recognise infections or particulates

56
Q

Do neutrophils have a short half-life?

A

Yes, (especially activated)

57
Q

What produces anti-inflammatory mediators to resolve acute inflammation? And what else do they do?

A

Macrophages (they also clear apoptotic cells)

58
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

59
Q

How do macrophages clear apoptotic cells?

A

They engulf them

60
Q

When does chronic inflammation occur?

A

When the acute response cannot clear the stimuli

61
Q

What does chronic inflammation result in?

A

Scarring and loss of tissue function

62
Q

What are some diseases characterised by chronic inflammation?

A

Rheumatoid arthritis
Asthma
Inflammatory bowel disease
Psoriasis
Multiple sclerosis

63
Q

What are some diseases associated with granulomatous inflammation?

A

Tuberculosis
Leprosy
Tumour reactions
Foreign body granuloma

64
Q

What are examples of persistent inflammatory stimulii?

A
  • persistent/ prolonged infection e.g., TB, hepatitis B/C
  • persistent toxic stimulii e.g., allergens, pollutants
  • unclearable particulates e.g., silica
  • autoimmunity e.g., self antigens
65
Q

What drive continual inflammation in chronic inflammation?

A

Antigens

66
Q

What are the distinct cell infiltrates in chronic inflammation?

A

inflammatory macrophages

T cells (and other lymphocytes)

Plasma (antibody secreting) cells

67
Q

Why is chronic inflammation a vicious cycle?

A

no clearance of inflammatory agent

Bystander tissue destruction

Concurrent repair processes (fibrosis and angiogenesis)

68
Q

Why is persistent neutrophil activation bad?

A

It is highly toxic and leads to rapid tissue destruction

69
Q

What is a foreign antigen?

A

an antigen derived from molecules not found in the body

70
Q

What is a self antigen?

A

An antigen derived from molecules produced by our bodies

71
Q

What is an immunogen?

A

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

72
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

73
Q

What is granulomatous inflammation?

A

Chronic inflammation with distinct patterns of granuloma formation

74
Q

How are macrophages recruited to the site of inflammation?

A

As monocytes, they can also be tissue residents

75
Q

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

A

Phagocytosis
Cytotoxic
Anti-inflammatory (e.g., TGF-B, IL-10)
Help repair wound by building ECM

76
Q

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

A

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

77
Q

What pro-inflammatory signals do T cells release?

A

TNF, IL-17 and IFN-gamma

78
Q

How do T cells promote remodelling and suppression of the immune system (aka act in a regulatory way)?

A

TGF-beta

79
Q

How do T cells act in a cytotoxic manner?

A

through the release of perforin and granzymes

80
Q

What do B cells do in an chronic inflammatory response?

A

Generate plasma cells that secrete antibodies that help to clear infection

81
Q

Which white blood cell can act remotely during chronic inflammation?

A

B cells

82
Q

What are granulomas?

A

Aggregation of activated macrophages

83
Q

What triggers granuloma formation?

A

Strong T cell responses

84
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

85
Q

What is granulomatous inflammation?

A

(type of chronic inflammation)
Inflammation with distinct pattern of granuloma formation

86
Q

What are the differences between acute and chronic inflammation?

A

Acute:

  • Rapid onset
  • Lasts a few days
  • Vasodilation
  • Neutrophils predominate
  • Histamine release
  • Prominent necrosis
  • Scarring
  • Either resolved or moves on to chronic inflammation

Chronic:

  • Delayed onset
  • Lasts years
  • Persistent inflammation
  • Ongoing tissue injury and attempts at healing
  • Monocytes and macrophages dominate
  • Ongoing cytokine release
  • Prominent scarring
  • Outcomes: scarring, loss of function
87
Q

What type of cell dominates during chronic inflammation?

A

Monocytes / Macrophages

88
Q

How long may a chronic inflammatory reaction last for?

A

Weeks, months or even years

89
Q

What is continually released during chronic inflammation?

A

Cytokine release

90
Q

What are the long term consequences of inflammation called?

A

The sequelae

91
Q

What are the three possible outcomes of injury?

A
  1. Regeneration
  2. Repair / scar formation
  3. Tissue scarring categorized by chronic inflammation
92
Q

What does resolution after injury involve?

A

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

93
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

94
Q

What is deposited when wounds heal?

A

ECM deposited

95
Q

How do scars form?

A

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

96
Q

Why does an inflammed area become hot?

A

the increased presence of fluid at core body temperature at a site that would otherwise have a limited exposure to this. During inflammation infiltrating immune cells are also highly metabolically active, which may also contribute to the generation of heat as a by-product.

97
Q

What are the positive outcomes of inflammation?

A

Clear inflammatory agent.
Remove damaged cells
Restore normal tissue function

98
Q

What are the negative outcomes of inflammation?

A

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

99
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

100
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

101
Q

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

A

TNF and IL-1

102
Q

Which epithelial ligand mediates transmigration of neutrophils to into the site of damage?

A

PECAM

103
Q

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

A

LFA-1 and MAC-1

104
Q

What are the consequences of inflammation?

A

Broncho-pneumonia
Scarring
Wound healing in sensitive tissues

POM Molecular Biology of the Cell (15 decks)

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