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1.1 POM Cells > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What are the 4 features of acute inflammation?

A
  1. Rubor (redness)
  2. Calor (heat)
  3. Tumor (swelling)
  4. Dolor (pain)
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2
Q

What is inflammation a response to?

A

Cellular injury

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3
Q

What is the purpose of inflammation?

A

Remove cause and consequence of cellular injury

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4
Q

What are the 6 causes of inflammation?

A
  1. Pathogen —> infection
  2. Allergen —> hypersensitivity (allergic reaction)
  3. Auto-antigens —> auto-immunity
  4. Physical damage —> trauma
  5. Extreme temperatures
  6. Necrosis or necroptosis (non-apoptotic cell death)
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5
Q

Which 6 types of disease can cause inflammation?

A
  1. Infection
  2. Autoimmunity
  3. Hypersensitivity
  4. Trauma
  5. Fibrotic disease
  6. Cancer
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6
Q

Which cells are involved in inflammation?

A
  1. Epithelial and endothelial —> release cytokines and chemokines for immune cell recruitment
  2. Neutrophils —> acute
  3. Macrophages —> chronic
  4. T and B lymphocytes
  5. Eosinophils and mast cells —> allergy
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7
Q

How is an acute inflammatory response activated?

A

Change in blood flow at site of injury —> structural changes in microvasculature —> accumulation of immune cells and proteins

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8
Q

Which tissues can acute inflammation effect?

A

Any vascularised tissue

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9
Q

What does tissue damage stimulate? (3)

A
  1. Inflammatory signals
  2. Vasodilator release
  3. Vascular changes
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10
Q

What do inflammatory signals stimulate?

A

Neutrophil recruitment

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11
Q

What are the 2 things identified via inflammatory signals?

A
  1. Foreign material
  2. Non-apoptotic cell death
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12
Q

What are the 2 vasodilators released at sites of injury?

A
  1. Histamine
  2. Nitrous oxide
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13
Q

What 2 main vascular changes occur at sites of tissue damage?

A
  1. Inc permeability
  2. Plasma leakage
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14
Q

What is the benefit of increased vascular permeability and leakage at sites of tissue damage?

A
  1. Inc antibodies
  2. Inc proteins
  3. Inc leukocyte migration
  4. Inc barrier —> doesn’t reach other tissues
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15
Q

Which 5 mediators are regulate inflammation at sites of injury?

A
  1. Histamine
  2. Prostaglandins
  3. Cytokines
  4. Chemokines
  5. Complement proteins
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16
Q

Which cells release prostaglandins at sites of inflammation? (2)

A
  1. Mast cells
  2. Leukocytes
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17
Q

Which cells release cytokines at sites of inflammation? (3)

A
  1. Macrophages
  2. Endothelial cells
  3. Mast cells
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18
Q

Which cells release chemokines at sites of inflammation? (3)

A
  1. Leukocytes
  2. Activated macrophages
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19
Q

What releases complement proteins at sites of inflammation? (3)

A

Plasma
(Proteins synthesised in liver)

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20
Q

Which cells release histamine at sites of inflammation? (3)

A
  1. Mast cells
  2. Basophils
  3. Platelets
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21
Q

What are the 3 functions of histamine in inflammation stimulation?

A
  1. Vasodilation
  2. Inc vascular permeability
  3. Endothelial activation
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22
Q

What is the function of prostaglandins in inflammation stimulation?

A

Vasodilation

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23
Q

What is the function of cytokines in inflammation stimulation?

A

Endothelial activation

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24
Q

What are the 2 functions of chemokines in inflammation stimulation?

A
  1. Chemotaxis —> immune cell recruitment
  2. Leukocyte activation
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25
Q

What are the 4 functions of complement proteins in inflammation stimulation?

A
  1. Chemotaxis —> immune cell recruitment
  2. Leukocyte activation
  3. Vasodilation
  4. Opsonisation —> phagocytosis
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26
Q

What is exudate?

A

Fluids, proteins and cells that have seeped out of the blood

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27
Q

What are the 3 stages of inflammation occurring?

A
  1. Steady state of tissue
  2. Damage occurs
  3. Immune cells recruited
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28
Q

How do chemokines recruit immune cells to sites of inflammation? (3)

A
  1. Released
  2. Diffuse —> gradient
  3. Leukocytes with complementary receptors migrate to chemokine source
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29
Q

Which immune cells are first recruited to sites of acute inflammation and how?

A

Neutrophils via IL-8 (CXCL8)

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30
Q

Which chemokine attracts neutrophils to sites of inflammation?

A

IL-8 (CXCL8)

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31
Q

What are the 4 steps of neutrophil extravasation?

A
  1. Chemo-attraction
  2. Rolling adhesion
  3. Tight adhesion
  4. Transmigration
32
Q

How does chemo-attraction work in neutrophil extravasation to sites of inflammation?

A

Cytokines stimulate endothelial upregulation of adhesion molecules (eg. selectins)
—> More for neutrophils to bind to on blood vessel wall

33
Q

How does rolling adhesion work in neutrophil extravasation to sites of inflammation?

A

Carbohydrate ligands of neutrophils bind to selectins
- Low affinity state
- eg. PSGL1 binds to P and E-selectins

34
Q

What do neutrophils bind in rolling adhesion?

A

Selectins

35
Q

How does tight adhesion work in neutrophil extravasation to sites of inflammation?

A

Chemokines promote low to high affinity switch in integrins
—> neutrophils bind stronger

36
Q

Which 2 integrins are switched in tight adhesion of neutrophils and why?

A

LFA-1 and Mac-1
—> enhances binding to ligands

37
Q

How does transmigration work in neutrophil extravasation to sites of inflammation?

A

Neutrophil cytoskeleton rearranges and pseudopodia formation (temporary extensions)
—> Diapedesis

38
Q

What mediates transmigration of neutrophils?

A

PECAM (Platelet Endothelial Cell Adhesion Molecule)

39
Q

What are the 3 functions of neutrophils at sites of inflammation?

A
  1. Pathogen recognition
  2. Pathogen clearance
  3. Cytokine secretion
40
Q

How do neutrophils recognise different gram -ve bacteria?

A

Use TLR4 and CD14 to identify different LPS (lipopolysaccharides) of bacteria

41
Q

How do neutrophils clear pathogens?

A
  1. Phagocytosis
  2. Netosis
42
Q

Why do neutrophils secrete cytokines at sites of inflammation?

A

Recruits and activates other immune cells

43
Q

What are 2 examples of enzymes in lysosomes?

A
  1. Lysozyme
  2. Elastase
44
Q

What are the 3 steps of phagocytosis?

A
  1. Endocytosis —> phagosome
  2. Fuse with lysosome —> phagolysosome
  3. Enzymes kill pathogen
    - Involves ROS (from phagocyte NADPH oxidase)
    - Involves antimicrobial peptides (eg. defensins)
45
Q

What are the parts of acute inflammation resolution?

A
  1. Neutrophil apoptosis (short half-life) and inflammatory mediator turn over
  2. Macrophages clear apoptotic cells
  3. Repair/wound healing
46
Q

What are the 3 types of inflammation?

A
  1. Acute
  2. Chronic
  3. Granulomatous
47
Q

What is granulomatous inflammation?

A

Chronic inflammation involving the formation of a granuloma

48
Q

What are some disease associated with chronic inflammation?

A
  1. Rheumatoid arthritis
  2. Asthma
  3. IBS
  4. MS
  5. Psoriasis
49
Q

What are some disease associated with granulomatous inflammation?

A
  1. TB
  2. Leprosy
  3. Crohn’s disease
50
Q

What are the 4 stimuli of chronic inflammation?

A

Persistent inflammatory stimuli
1. Prolongued infection
2. Persistant toxic stimuli (allergens/pollutants)
3. Unclearable particulates (eg. silica)
4. Autoimmunity —> always self-antigens in body

51
Q

Which 3 cells are involved in chronic inflammation?

A
  1. Macrophages
  2. T cells
  3. Plasma cells
52
Q

When will chronic inflammation occur? (2)

A
  1. No clearance of inflammatory agent
  2. Bystander tissue destruction
  3. Concurrent tissue repair —> fibrosis and angiogenesis
53
Q

How are macrophages recruited to sites of chronic inflammation?

A

Tissue-resident or as monocytes in blood

54
Q

What are the benefits of macrophages in chronic inflammation?

A
  1. Phagocytosis
  2. Cytotoxic
  3. Anti-inflammatory chemical release
  4. Wound repair
55
Q

What are the negative consequences of macrophages in chronic inflammation?

A
  1. Cytotoxic —> damage
  2. Inflammatory
  3. Pro-fibrotic
56
Q

What are the 3 types of T cells found at sites of chronic inflammation?

A
  1. Pro-inflammatory (Th1 and Th17)
  2. Cytotoxic T cells
  3. Treg cells (Th0)
57
Q

What do pro-inflammatory T cells release at sites of chronic inflammation and why? (3)

A
  1. TNF
  2. IL-17
  3. IFN-γ
    - Recruits neutrophils and macrophages
    - Activates macrophages
58
Q

What do cytotoxic T cells release at sites of chronic inflammation and why?

A
  1. Granzymes
  2. Perforin
  3. Granule-associated proteins
    - Kill infected cells
59
Q

What do Treg cells release at sites of chronic inflammation and why?

A
  1. TGF-β
  2. IL-10
    - Immunosuppressive —> regulate inflammation
60
Q

How do B cells contribute to chronic inflammatory?

A

Generate plasma cells —> antibodies

61
Q

Do B cells always travel to the site of chronic inflammation?

A

No - may operate remotely

62
Q

What is a granuloma?

A

Distinct circle of aggregated macrophages

63
Q

What is the trigger of granuloma formation?

A

Strong T cell response to resistant agents

64
Q

What are the 6 differences between acute and chronic inflammation?

A
  1. Time - onset and duration
  2. Effects
  3. Predominant cells
  4. Chemicals released
  5. Prominent feature
  6. Outcomes
65
Q

What is the difference between the onset time of acute and chronic inflammation?

A
  • Acute —> immediate
  • Chronic —> delayed
66
Q

What is the difference between the duration of acute and chronic inflammation?

A
  • Acute —> days
  • Chronic —> weeks to years
67
Q

What is the difference between the effects of acute and chronic inflammation?

A
  • Acute —> vasodilation, inc vascular permeability, leukocyte response
  • Chronic —> perisistent inflammation, attempts at healing
68
Q

What is the difference between the predominant cells involved in acute and chronic inflammation?

A
  • Acute —> neutrophils
  • Chronic —> macrophages
69
Q

What is the difference between the main chemicals released in acute and chronic inflammation?

A
  • Acute —> histamine
  • Chronic —> ongoing cytokine release
70
Q

What is the difference between the prominent visual feature of acute and chronic inflammation?

A
  • Acute —> necrosis
  • Chronic —> scarring (attempt at healing)
71
Q

What is the difference between the outcomes of acute and chronic inflammation?

A
  • Acute —> complete resolution or progresses to chronic
  • Chronic —> scarring and tissue function loss
72
Q

What are the 3 possible positives of inflammation?

A
  1. Can clear inflammatory agent
  2. Removes damaged cells
  3. Can restore normal tissue function
73
Q

What are the 3 possible negatives of inflammation

A
  1. May cause excess tissue damage
  2. May cause scarring
  3. May lose organ function —> organ failure
74
Q

What does post-inflammatory wound healing lead to?

A

ECM deposition

75
Q

What is sequelae?

A

Aftereffects

1.1 POM Cells (15 decks)

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