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POM 2 Cell biology > 2.13 Inflammation > Flashcards

2.13 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 at a site of inflammation?

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 generates heat

Increased presence of fluid at core body temperature in areas with usually limited exposure

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4
Q

What causes pain at a site of inflammation?

A

Some mediators that signal to immune and endothelial cells during inflammation also signal to local nerve cells

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5
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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6
Q

What are the causes of inflammation?

A

Pathogens, allergens, physical damage, extreme temperatures, autoantigens

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7
Q

Where can inflammation occur?

A

Any vascularised tissue

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8
Q

When is inflammation initiated?

A

When cellular damage leads to release of damage associated molecular patterns

Or body detects pathogen associated molecular patterns

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9
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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10
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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11
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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12
Q

What is acute inflammation characterised by?

A

Neutrophil recruitment

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13
Q

What triggers the release of DAMPs and PAMPs?

A

Non-apoptotic cell death (e.g. a wound)

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14
Q

What vasodilators do mast cells release?

A

Nitric oxide and histamine

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15
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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16
Q

Outline what happens when cell damage occurs

A
  1. Non-apoptotic cell death occurs, foreign material is detected
  2. Immune cells are activated by DAMPs or PAMPs, and mast cells release histamine and nitric oxide (vasodilators)
  3. Rapid vasculature changes occur (permeability, leakage, vasodilation)
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17
Q

What 4 benefits does increased vascular permeability and leakage into a site of inflammation bring? BALP

A

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

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18
Q

Why do we experience pain during inflammation?

A

Due to the release of prostaglandins

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19
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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20
Q

What is exudate?

A

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

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21
Q

What does the exudate form?

A

Physical barrier between healthy and inflamed tissue

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22
Q

How are neutrophils able to migrate towards the chemokine source?

A

They express complementary chemokine receptors which allow them to migrate to the site of damage where chemokines are produced

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23
Q

What receptors bind to the chemokine CXCL8 (interleukin-8)?

A

CXCR1 and CXCR2 (g-coupled membrane proteins)

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24
Q

Which cell type prominently expresses receptors that bind to CXCL8 (IL-8) and what does this mean?

A

Neutrophils, thus they are the first cell type to be recruited to the site of inflammation

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25
What is meant by neutrophil extravasation?
The movement of neutrophils from the **vasculature into the surrounding tissue** to reach the site of inflammation
26
What are the four steps of neutrophil extravasation?
1. Chemo-attraction 2. Rolling adhesion 3. Tight adhesion 4. Transmigration
27
What are the two adhesion molecules which are upregulated by cytokines?
P-selectin and E-selectin
28
How do neutrophils recognise selectin molecules on the endothelium?
They have complementary carbohydrate ligands which bind to the selectin molecules
29
What is chemo-attraction?
**Cytokines** (e.g. TNF-a) act on the endothelial layer to promote upregulation of **adhesion molecules** (e.g. selectins)
30
What is rolling adhesion?
**Ligands** (e.g. PSGL1) in a low affinity state on neutrophils bind **selectin** molecules, causing the neutrophil to roll along the endothelium
31
What is the name of the P selectin ligand?
PSGL1
32
What promotes the low to high affinity switch in integrins in tight adhesion and what does this do?
Chemokines This enhances binding to ligands (e.g. ICAM-1)
33
What is transmigration?
The movement of the neutrophil through the endothelial wall which involves the rearrangement of the **cytoskeleton**
34
What molecule mediates the transmigration of the neutrophil molecule?
PECAM
35
What are the three functions of neutrophils at the site of inflamation?
1. Pathogen recognition 2. Pathogen clearance 3. Cytokine secretion
36
How do neutrophils recognise gram negative bacteria?
They use **TLR4 and CD14 receptors** to identify **lipopolysaccharides** that are present in gram negative bacteria
37
How do neutrophils clear pathogens?
By phagocytosis
38
Describe the process of phagocytosis?
1. Pathogen is engulfed into **phagosome** 2. Phagosome fuses with enzyme containing vesicles forming a **phagolysosome** 3. This is **degraded by enzymes** through acidifcation
39
What is released during phagocytosis which causes oxidative damage?
ROS - reactive oxygen species
40
Give 3 reasons why the release of exudate is helpful?
Increases **lymphatic drainage** Allow direct delivery of **plasma proteins** (e.g. fibrin) to inflammation site Forms **physical barrier** between healthy and inflamed tissue
41
Why are histamine molecules turned over rapidly?
They are small molecules and therefore are rapidly degraded
42
What produces anti-inflammatory mediators to resolve acute inflammation?
Macrophages
43
How can acute inflammation be resolved through repair?
Infiltrating WBCs **clear the wound** of dead cells and pathogens They also release **growth factors** which stimulate tissue repair via **ECM deposition**
44
How do macrophages clear apoptotic cells?
They engulf them
45
When does chronic inflammation occur?
When the acute response cannot clear the stimuli
46
What does chronic inflammation result in?
Scarring and loss of tissue function
47
What drive continual inflammation in chronic inflammation?
Antigens
48
Why is persistent neutrophil activation bad?
It is highly toxic and leads to rapid tissue destruction
49
What is a foreign antigen?
An antigen derived from molecules not found in the body
50
What is a self antigen?
An antigen derived from molecules produced by our bodies
51
What is an immunogen?
An antigen indepedently capable of driving an immune response in the absence of additional substances
52
What is a hapten?
A small molecule that **alone** does **not act as an antigen** but when **bound** to a larger molecule it can **create an antigen**
53
What is granulomatous inflammation?
Chronic inflammation with distinct patterns of granuloma formation
54
Name some diseases characterised by chronic inflammation?
Rhuematoid Arthritis Asthma Inflammatory Bowel Disease Hepatitis Psoriasis
55
Name some diseases associated with granulomatous inflammation?
TB Leprosy Tumour reactions Crohn's Disease
56
What are some persistent inflammatory stimuli found in chronic inflammation? TUPS
**T**oxic stimuli (e.g. allergens and pollutants) **U**nclearable particulates **P**ersistent/prolonged infection **S**elf-antigens
57
What does the distinct immune cell infiltrate found in chronic inflammation consist of?
Inflammatory macrophages T cells Plasma cells
58
How are macrophages recruited to the site of inflammation?
As monocytes
59
What are the benefits of macrophages being recruited to the site of inflammation? PCAR
**P**hagocytosis **C**ytotoxic effect **A**nti-inflammatory **R**epair wound by building ECM
60
What are the bad things associated with macrophages being recruited to the area? DIP
**D**amage healthy surrounding tissue **I**nflammatory **P**ro-fibrotic, deposit excess collagen
61
What pro-inflammatory signals do T cells release?
TNF, IL-17 and IFN-gamma
62
How do T cells promote remodelling and suppression of the immune system?
TGF-beta
63
How do T cells act in a cytotoxic manner?
Through the release of perforin and granzymes
64
What do B cells do in an chronic inflammatory response?
Generate antibodies that help to clear infection
65
Which white blood cell can act remotely during chronic inflammation?
B cells
66
What are granulomas?
Aggregations of **activated macrophages**
67
What triggers granuloma formation?
Strong T cell responses
68
What is the job of the granulomas?
To form a **physical barrier** to prevent pathogenic material from leaking out, thus allowing macrophages to **clear the material**
69
Compare acute and chronic inflammation in terms of onset
Acute is rapid, lasts a few days Chronic is delayed, lasts up to years
70
What type of cell dominates during acute vs chronic inflammation?
Acute – neutrophils Chronic – monocytes/macrophages
71
What is continually released during acute vs chronic inflammation?
Acute – histamines Chronic – cytokines
72
What happens as a result of acute vs chronic inflammation?
Acute – vasodilation, vascular permeability, leukocyte response Chronic – persistent inflammation, ongoing injury, attempts at healing
73
What are the long term consequences of inflammation called?
The sequelae
74
What are the three possible outcomes of injury?
1. Regeneration 2. Repair/scar formation 3. Tissue scarring categorized by chronic inflammation
75
What does resolution after injury involve?
The clearance of injurious stimuli and inflammatory mediators Replacing injured cells Returning to normal function
76
What does fibrosis involve as an sequalae of inflammation?
the deposition of collagen leading to excess tissue scarring and therefore the inability of the tissue to carry out its function
77
What is deposited when wounds heal?
ECM deposited
78
How do scars form?
When the collagen is unable to be removed from the site of endothelial repair
79
What are the positive outcomes of inflammation?
Clear inflammatory agent Remove damaged cells Restore normal tissue function
80
What are the negative outcomes of inflammation?
Excess tissue damage Scarring Loss of organ function -> organ failure
81
Describe how neutrophils are able to migrate through the blood vessel walls?
Through the relaxation of inter-endothelial cell junctions and digestion of vascular basement membrane
82
Which chemokines released by macrophages cause chemo-attraction of neutrophils to the site of injury?
TNF and IL-1
83
Which epithelial ligand mediates transmigration of neutrophils to into the site of damage?
PECAM
84
Which chemokines cause the switch from low affinity ligands to high affinity ligands?
LFA-1 and MAC-1

POM 2 Cell biology (15 decks)

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