1.1 POM Cells > Inflammation > Flashcards

Inflammation Flashcards

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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
What are the 4 functions of complement proteins in inflammation stimulation?
1. Chemotaxis ---> immune cell recruitment 2. Leukocyte activation 3. Vasodilation 4. Opsonisation ---> phagocytosis
26
What is exudate?
Fluids, proteins and cells that have seeped out of the blood
27
What are the 3 stages of inflammation occurring?
1. Steady state of tissue 2. Damage occurs 3. Immune cells recruited
28
How do chemokines recruit immune cells to sites of inflammation? (3)
1. Released 2. Diffuse ---> gradient 3. Leukocytes with complementary receptors migrate to chemokine source
29
Which immune cells are first recruited to sites of acute inflammation and how?
Neutrophils via IL-8 (CXCL8)
30
Which chemokine attracts neutrophils to sites of inflammation?
IL-8 (CXCL8)
31
What are the 4 steps of neutrophil extravasation?
1. Chemo-attraction 2. Rolling adhesion 3. Tight adhesion 4. Transmigration
32
How does chemo-attraction work in neutrophil extravasation to sites of inflammation?
Cytokines stimulate endothelial upregulation of adhesion molecules (eg. selectins) ---> More for neutrophils to bind to on blood vessel wall
33
How does rolling adhesion work in neutrophil extravasation to sites of inflammation?
Carbohydrate ligands of neutrophils bind to selectins - Low affinity state - eg. PSGL1 binds to P and E-selectins
34
What do neutrophils bind in rolling adhesion?
Selectins
35
How does tight adhesion work in neutrophil extravasation to sites of inflammation?
Chemokines promote low to high affinity switch in integrins ---> neutrophils bind stronger
36
Which 2 integrins are switched in tight adhesion of neutrophils and why?
LFA-1 and Mac-1 ---> enhances binding to ligands
37
How does transmigration work in neutrophil extravasation to sites of inflammation?
Neutrophil cytoskeleton rearranges and pseudopodia formation (temporary extensions) ---> Diapedesis
38
What mediates transmigration of neutrophils?
PECAM (Platelet Endothelial Cell Adhesion Molecule)
39
What are the 3 functions of neutrophils at sites of inflammation?
1. Pathogen recognition 2. Pathogen clearance 3. Cytokine secretion
40
How do neutrophils recognise different gram -ve bacteria?
Use TLR4 and CD14 to identify different LPS (lipopolysaccharides) of bacteria
41
How do neutrophils clear pathogens?
1. Phagocytosis 2. Netosis
42
Why do neutrophils secrete cytokines at sites of inflammation?
Recruits and activates other immune cells
43
What are 2 examples of enzymes in lysosomes?
1. Lysozyme 2. Elastase
44
What are the 3 steps of phagocytosis?
1. Endocytosis ---> phagosome 2. Fuse with lysosome ---> phagolysosome 3. Enzymes kill pathogen - Involves ROS (from phagocyte NADPH oxidase) - Involves antimicrobial peptides (eg. defensins)
45
What are the parts of acute inflammation resolution?
1. Neutrophil apoptosis (short half-life) and inflammatory mediator turn over 2. Macrophages clear apoptotic cells 3. Repair/wound healing
46
What are the 3 types of inflammation?
1. Acute 2. Chronic 3. Granulomatous
47
What is granulomatous inflammation?
Chronic inflammation involving the formation of a granuloma
48
What are some disease associated with chronic inflammation?
1. Rheumatoid arthritis 2. Asthma 3. IBS 4. MS 5. Psoriasis
49
What are some disease associated with granulomatous inflammation?
1. TB 2. Leprosy 3. Crohn's disease
50
What are the 4 stimuli of chronic inflammation?
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
Which 3 cells are involved in chronic inflammation?
1. Macrophages 2. T cells 3. Plasma cells
52
When will chronic inflammation occur? (2)
1. No clearance of inflammatory agent 2. Bystander tissue destruction 3. Concurrent tissue repair ---> fibrosis and angiogenesis
53
How are macrophages recruited to sites of chronic inflammation?
Tissue-resident or as monocytes in blood
54
What are the benefits of macrophages in chronic inflammation?
1. Phagocytosis 2. Cytotoxic 3. Anti-inflammatory chemical release 4. Wound repair
55
What are the negative consequences of macrophages in chronic inflammation?
1. Cytotoxic ---> damage 2. Inflammatory 3. Pro-fibrotic
56
What are the 3 types of T cells found at sites of chronic inflammation?
1. Pro-inflammatory (Th1 and Th17) 2. Cytotoxic T cells 3. Treg cells (Th0)
57
What do pro-inflammatory T cells release at sites of chronic inflammation and why? (3)
1. TNF 2. IL-17 3. IFN-γ - Recruits neutrophils and macrophages - Activates macrophages
58
What do cytotoxic T cells release at sites of chronic inflammation and why?
1. Granzymes 2. Perforin 3. Granule-associated proteins - Kill infected cells
59
What do Treg cells release at sites of chronic inflammation and why?
1. TGF-β 2. IL-10 - Immunosuppressive ---> regulate inflammation
60
How do B cells contribute to chronic inflammatory?
Generate plasma cells ---> antibodies
61
Do B cells always travel to the site of chronic inflammation?
No - may operate remotely
62
What is a granuloma?
Distinct circle of aggregated macrophages
63
What is the trigger of granuloma formation?
Strong T cell response to resistant agents
64
What are the 6 differences between acute and chronic inflammation?
1. Time - onset and duration 2. Effects 3. Predominant cells 4. Chemicals released 5. Prominent feature 6. Outcomes
65
What is the difference between the onset time of acute and chronic inflammation?
- Acute ---> immediate - Chronic ---> delayed
66
What is the difference between the duration of acute and chronic inflammation?
- Acute ---> days - Chronic ---> weeks to years
67
What is the difference between the effects of acute and chronic inflammation?
- Acute ---> vasodilation, inc vascular permeability, leukocyte response - Chronic ---> perisistent inflammation, attempts at healing
68
What is the difference between the predominant cells involved in acute and chronic inflammation?
- Acute ---> neutrophils - Chronic ---> macrophages
69
What is the difference between the main chemicals released in acute and chronic inflammation?
- Acute ---> histamine - Chronic ---> ongoing cytokine release
70
What is the difference between the prominent visual feature of acute and chronic inflammation?
- Acute ---> necrosis - Chronic ---> scarring (attempt at healing)
71
What is the difference between the outcomes of acute and chronic inflammation?
- Acute ---> complete resolution or progresses to chronic - Chronic ---> scarring and tissue function loss
72
What are the 3 possible positives of inflammation?
1. Can clear inflammatory agent 2. Removes damaged cells 3. Can restore normal tissue function
73
What are the 3 possible negatives of inflammation
1. May cause excess tissue damage 2. May cause scarring 3. May lose organ function ---> organ failure
74
What does post-inflammatory wound healing lead to?
ECM deposition
75
What is sequelae?
Aftereffects
1.1 POM Cells
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