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PATH30001 - Mechanisms of Disease > Lecture 6 - Inflammation > Flashcards

Lecture 6 - Inflammation Flashcards

1
Q

What are the aims of inflammation?

A
  • dilute
  • destroy
  • isolate
  • initiate repair
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2
Q

What are the two forms of inflammation?

A

Acute

Chronic

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3
Q

Which are the most important cells in inflammation?

A
  • endothelial cells

* neutrophils

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4
Q

What are the most important mediators of inflammation?

A

Cytokines

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5
Q

What is the general function of the mediators?

A

To initiate the inflammatory response

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6
Q

Where do the chemical mediators of inflammation come from?

A
  • cells

* plasma proteins

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7
Q

Describe amplification of mediators

A

One mediator is activated
This mediator then goes on to activate many more
(a cascade)

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8
Q

Why do the chemical mediators have a short half life?

A

Don’t want inflammation to continue on unregulated.

We want this to be a short response

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9
Q

Describe the sequence of events in acute inflammation

A

→ Injury

  1. Vasodilation
  2. Vascular leakage and oedema
  3. PMN migration
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10
Q

What are some other names for neutrophils?

A

Polymorphs

PMNs

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11
Q

What is the benefit of oedema?

A

Dilute the toxins/pathogens

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12
Q

Describe the effects of vasodilation

A

• PMNs are able to migrate out
• Fluid leakage; transudate initially
→ later exudate
• Increased interstitial osmotic pressure

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13
Q

What is transudate?

A

Protein-poor filtrate

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14
Q

What is the effect of increased interstitial osmotic pressure?

A

Increases oedema

water wants to move out of the capillaries

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15
Q

Describe Retraction

A
  • Endothelial cells pull apart from each other
  • Cytoskeletal reorganisation

Brought about by
• TNF
• IL-1

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16
Q

What brings about increased vascular permeability?

A

Histamines

+ Bradykinins, Leukotrienes

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17
Q

How long does increased vascular permeability take?

A

15-30 mins

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18
Q

Which severe injuries can bring about endothelial damage?

A

Heat
UV injury
Bacterial toxins

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19
Q

What is transcytosis?

A

No change in junctions of endothelial cells
Membrane permeability increases
Flow of fluids through the cells using vesicles

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20
Q

What causes transcytosis?

A

VEGF: vascular endothelial growth factor

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21
Q

Which things can induce damage of endothelial cells?

A

Toxins
Bacteria
Immune cells
• e.g. Macrophages producing free radicals and proteolytic enzymes

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22
Q

Why do macrophages release proteolytic enzymes?

What is the result?

A

In an attempt to destroy pathogens

However, the enzymes can also damage the endothelial cells

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23
Q

Describe neutrophil recruitment

A
  1. Margination & rolling
    • E and P selectin mediated
    • Transient interactions
  2. Adhesion
    • Integrin mediated
    • ICAM-1 and VCAM-1 on endothelial cells
    • LFA-1 and VLA-4 on neutrophils
  3. Diapedesis
    • PECAM-1 homotypic interactions
  4. Chemotaxis
    • CXCL8
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24
Q

What is the effector function of neutrophils?

A
  • Phagocytosis
  • Degranulation
  • Mopping up debris (phagocytosis)
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25
What are in the neutrophil granules?
Anti-microbial compounds * Proteolytic enzymes * Defensins
26
Describe the sequence of events in acute inflammation
1. Oedema 2. Neutrophils 3. Monocytes / macrophages
27
Describe how neutrophils are 'selected out'
Rolling: In the area of inflammation the endothelial cells start expressing Selectin molecules on their surface These molecules bind transiently to Sialyl-Lewis X on the neutrophil
28
Which chemical mediator up-regulates selectin expression on endothelial cells?
Histamine | Thrombin
29
What causes margination?
Crowding and engorged circulation
30
Where is ICAM-1? | What does it bind?
It's on the endothelium | It binds LFA on the neutrophil
31
Where is P-selectin? | What does it bind?
On the endothelium | It binds Sialyl-Lewis X
32
What is the receptor responsible for diapedesis? | Describe the receptor interaction
PECAM-1 Found on both neutrophil and endothelium Self-interaction
33
What is another name for diapedesis?
Transmigration
34
How do neutrophils know where to go after diapedesis?
Chemotaxis
35
What is a really important cytokine for chemotaxis? | Describe what happens
IL-8 This is a cytokine subfamily * IL-8 released by inflammatory cells * IL-8R on neutrophils engaged * Polarisation of the neutrophil * Cytoskeletal rearrangements in neutrophils and migration towards the source of inflammation
36
What are some generic chemo-attractants?
* Bacterial products (LPS) * Complement * Chemokines (IL-8)
37
What are the two derivations of chemical mediators of inflammation?
* Cell derived | * Plasma derived
38
Describe plasma derived mediators
Often enzymes that require activation
39
Which plasma proteins are important chemical mediators of inflammation?
Complement system Kinin system Clotting system Fibrinolytic system
40
Which chemical mediator systems are important?
* Plasma proteins * Arachidonic acid metabolites * cytokines and chemokines * vasoactive amines
41
What initiates the plasma chemical mediator system? What initiates this?
Factor XII • Hageman factor Hageman factor triggered by Activated platelets
42
What does Factor XII trigger? What is important about this?
Kinin cascade Clotting cascade Fibrinolytic system Complement cascade It is important to note that these systems are all interrelated
43
Which mediator is produced by the kinin cascade? | Discuss this
``` Bradykinin • Increases vascular permeability and arteriolar dilation • Causes pain • bronchial smooth muscle contraction • rapidly inactivated ```
44
Which factor is produced by the clotting cascade? | What is its role in inflammation?
Thrombin Role: 1. Fibrin clot formation • Soluble fibrinogen → Insoluble fibrin clot 2. Expression of Selectins on endothelium for leukocyte recruitment
45
Which complement derivatives have a direct impact on the inflammatory response? What is their effect?
"Anaphalotoxins" * C3a * C5a Recruitment of white blood cells
46
What is the most important vasoactive amine?
Histamine
47
Describe the action of Histamine Which cells release it?
Function: • Endothelial cell contraction (increased vascular permeability) • Increased expression of selections on endothelium Derived from: • Mast cells • Basophils
48
Describe the action of Nitric oxide (NO)
* Bronchodilation * Vasodilation • Regulation of thrombus
49
What are some arachidonic acid metabolites? | What is their function?
``` 1. Prostacyclin • vasodilation 2. Thromboxane • vasoconstriction 3. Leukotrienes 4. PAF ```
50
Which drugs target the arachidonic acid pathway?
NSAIDS • They target COX (important in this pathway) Steroid • Targets Phospholipases • More potent anti-inflammatory effect
51
What type of mediator are leukotrienes?
Arachidonic acid metabolite
52
What are eicosanoids?
aka Arachidonic acid metabolites
53
What is the effect of glucocorticoids (steroids) on inflammation?
Inhibit arachidonic acid metabolite production through targeting of Phospholipases Very potent response (because it inhibits stuff early on in the pathway)
54
Where do NSAIDS affect the Arachidonic acid pathway?
COX This is further down the pathway Thus is less potent
55
Which is the major inhibitory interleukin?
IL-10
56
How can we inhibit acute inflammation through cytokines?
* more IL-10 * reduce cells producing cytokines * reduce circulating cytokines with Mabs * receptor blockade with antagonists or mabs
57
What are some systemic effects of acute inflammation?
* fever | * leukocytosis
58
What is leukocytosis?
Elevated white blood cell count
59
Which mediators suppress inflammation?
(Endogenous) Glucocorticoids | IL-10
60
What is PAF?
Platelet activating factor
61
Describe the vasodilation / constriction interaction between two of the AA metabolites
Prostacyclin • Vasodilation Thromboxane • Vasoconstriction

PATH30001 - Mechanisms of Disease (34 decks)

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