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Unit 9 > Physiology of Inflammation > Flashcards

Physiology of Inflammation Flashcards

1
Q

What are the 3 phases of inflammation?

A

INITIATION:
- stimulus + recognition = local production of inflammatory mediators

PATENT INFLAMMATION PROCESS:
RESOLUTION:
- Local dilation of capillaries = increased blood flow
- Microvascular structural changes and plasma proteins escape from blood
- Leukocytes accumulate at injury site

RESOLUTION:
- Removal of stimulus
- Inhibitory feedbacks and counter-balanced cellular and humour response
- Repair and if adaptive immunity engaged we get memory development

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2
Q

What are the 2 ways inflammation is defined?

A

1- Morphological pattern
* Serous inflammation
* Fibrinous inflammation
* Haemorrhagic inflammation
* Suppurative (purulent) inflammation
*Necrotising (gangrenous) inflammation
* Ulcers

2- Classification of inflammation
* Acute – fast onset, prominent signs, mild outcomes and self-limited
* Chronic – slow onset, less prominent signs & severe outcomes and progressive disease

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3
Q

Describe the steps in the key inflammatory process. (8)

A

1- Stimulus occurrence
2- Stimulus recognition
3- Vasodilation
4- Vascular permeability changes
5- Cell recruitment
6- Cell activation
7- Cell extra-vasation
8- Repair/resolution

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4
Q

What are different ways in which non-self antigens can be indentified?

A

1- Humoral factors
* Complement system * Antibodies *Other proteins e.g. LBP

2- Innate cell recognition (mostly due to immune cells)
* PRRs
* complement and antibody
responses

3- Adaptive immuno-recognition
* Specific responses (depending on individual immune history)

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5
Q

How is a stimulus recognised innately?

A
  • PRRs (pattern recognition receptors) detect:

1- PAMPs (pathogen-associated molecular patterns)
2- DAMPs (damage-associated molecular patterns)
3- LAMPs/MAMPs,
(lifestyle- and metabolism- associated molecular patterns)
4- SAMPs, (self/suppression-associated molecular patterns)

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6
Q

What do the different PRRs detect?

A

TLRs - anything
CLRs ( c-type lectin) - fungi
RLRs - viral RNA
NODs - bacteria

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7
Q

What do we mean by homeostasis of inflammation?

A

We need more SAMPs than DAMPs to return back to normal and inflammation to stop.

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8
Q

What happens once the stimulus has been recognised?

A

Initial mediator release (at first locally)

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9
Q

What causes vasodilation?

A
  • Mainly due to Histamine and NO, released by Mast cells and macrophages
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10
Q

1- Why does vascular permeability change?
2- Vasodilation and vascular permeability increase causes what to happen?

A

1- Mainly due to Histamine, released by Mast cell

2- Endothelial cells retraction and rearrangement of tight-junctions, forming gaps between them and allowing fluid exudation - Loss of protein leads to oedema (swelling)

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11
Q

What are the mediators of inflammation?
hints:
- Amines
- Lipids
- Peptides+ Proteins
- Small molecules

A
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12
Q

Where is histamine released from?
What is its function in inflammation?
What does it bind to?
Histamine has great importance in…

A

– Released from mast cells
–> dilate blood vessels + increase microvascular permeability
-> G-protein coupled receptors (H1)
-> Asthma and allergies

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13
Q

How are lipids mediators of inflammation?

A
  • Cell undergoes Inflammatory stimuli:
    Phospholipid targeted by
    phosphorylated Phospholipase A2 = Arachidonic acid (omega 6 fatty acid) + Lyso-glyceryl phosphorylcholine
  • Arachidonic acid (AA) is a precursor to several pro-inflammatory lipid mediators, including prostaglandins and leukotrienes.
  • Lyso-glyceryl phosphorylcholine acts as an intermediate in Platelet activating factor formation
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14
Q

What cells produce PAF? (5)
- How is it made?

A

Platelets, mast cells, neutrophils, macrophages, endothelial cells

-> Enzymatic conversion of lyso-PAF to PAF through acetylation.

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15
Q

When platelet activation factor binds to PAF-receptors what happens? (7)
(PAF is a potent mediator of inflammation)

A

1- Strong Vasodilation + vascular permeability more potent than Histamine
2- Bronchoconstriction
3- Platelet aggregation and degranulation
4- Leukocyte chemotaxis, extravasatio
5- Promote Neutrophil oxidative burst
6- Increase production of eicosanoids by inducing
Cox2 transcription
7- Increase transcription of IL6, MMPs, iNOS

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16
Q

What are Eicosanoids? Docosanoids?
What is significant about Eicosapentaenoic acid?

A
  • Eicosanoids = lipid molecules derived from arachidonic acid, a 20-carbon polyunsaturated fatty acid.
  • Docosanoids, as the name suggests, are derived from docosahexaenoic acid (DHA) 22 carbons
    > Includes molecules such as resolvins, protectins and Maresins
  • EPA, while also an omega-3 fatty acid, is a 20-carbon molecule, so it does not fit into either the eicosanoid or docosanoid categories.
    > Includes Resolvins
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17
Q

What molecules are derived from Aracadonic acid? “Eicosanoids”

A

1- Epoxy-Eicosa Tetraenoid acids (EETs)
2- Prostaglandins, Prostacyclins and Thromboxanes
3- Leukotrienes
4- Lipoxins (anti inflammatory)
5- “Isoprostanes due to oxidative stress”

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18
Q

How are Ecosanoids produced?

A
  • Consumption of essential fatty acids:
    a-linolenic acid (omega-3 fatty acid) and linoleic acid (omega-6 fatty acid)
19
Q

Why are EPA and DHA important?

A
  • Omega 3 fatty acids involved in the production of anti-inflammatory molecules.
  • Promote healing after danger removed
    > DHA: resolvins, maresins, protectins
    > EPA: resolvins
20
Q

What does the effect of Eicosanoids depend on? (2)

A

1- Half life
2- Type of receptors they interact with … therefore the type of cells and tissues

21
Q

True/False Eicosanoids are fundamentally important in mediating inflammatory response locally and systemically but also important in physiological daily mechanisms?

A

TRUEEEEEE

22
Q

Each cell type has a different set of eicosanoids synthetic enzymes, what does this mean?

A
  • Specific enzymes expressed by the cell determine which type of eicosanoid IS synthesized. (each cell type has a different set of eicosanoids receptors/responses)
  • Ensures that eicosanoids are generated in response to specific physiological needs and helps maintain tissue and systemic homeostasis.
23
Q

We need to maintain equilibria of Eicosanoids. (we have intrinsic regulatory mechanisms and delicate equilibria to contain their effects)

  • PGE2 is produced by mast cells and macrophages what contains the effect of PGE2?
A

Prostacycline PGI2 produced by vascular cells

PGI2: PGI2 has anti-inflammatory properties
PGE2: PGE2 has a more complex role in inflammation.

24
Q

The thromboxane produced by platelets, TxA2 is unstable and hydrolysed to TxB2 becomes inactive.
What is TxA2 physiological antagonist?

A

The prostacyclin PGI2
opposite effect to regulate systemic blood pressure and thrombogenesis

25
Q

What are the adverse effects of blocking Cox 2?

A
  • Cox-2 allows production PGI2 which has anticoagulant effects
  • Cox-1 needed by platelets for platelet aggregation which produces TXA2 which has pro coagulatory effect and thrombotic effect
    > If thrombotic effect not counteracted by PGI2 = CV problems
26
Q

What do NSAIDs do?

A

Inhibit cyclooxygenase enzymes (Cox1 and Cox2)
* Cox- 2 Block synthesis of PGs and TXs
- Cox-2 induced in inflammation so needs to be targeted to reduce inflammation

  • Cox-1 inhibit platelet agg + increased gastric secretion + reduced renal blood flow
27
Q

What is the function of cyclooxygenase?
What is the function of lipoxygenase

A
  • Control the production of prostaglandins, prostacyclin’s and thromboxane’s
  • Control production of leukotrienes and lipoxins
28
Q

Why does cox-1 inhibition cause peptic ulcers and GI bleeding?

A

Need PGE2 for gastric protection
- Mucus secretion
- Bicarbonate
- Mucosal blood flow

Causes increased gastric acid secretion;
– reduced gastric/duodenal mucus/HCO3- secretion= risk of GI ulceration
* always consider prescribing PPI for gastro-protection or using co- formulation (e.g. naproxen + esomeprazole)

29
Q

What is the relationship of Lipokins and leukotrienes?

A
  • Lxs and Lks do the opposite
    Lxs control the resolution of inflammation by stopping neutrophils
    Lks are pro inflammatory
  • Physiological antagonist acting on the same receptors but different effect
30
Q

Why is it important to have a healthy diet of anti-oxidants?

A
  • Arachidonic acid becomes Isoprostanes under oxidative stress
  • Isoprostanes have casocontrictive effects and activate NK cells
    > No counteracting molecule and so are not balanced so can be dangerous
31
Q

Name the active and inactive form of Glucocorticoids.

A

Active: Hydrocortisone Cortisol
Inactive: Cortisone

32
Q

How do Glucocorticoids work?

A
  • Bind to cytoplasmic GR receptors, normally inactive and associated to HSPs
  • Upon binding HSP dissociate and activated receptors dimerize
  • Dimer of Activated receptors translocate to nucleus
  • In the nucleus dimers bind to DNA-motifs called glucocorticoid response elements (GRE)
  • Gene transcription modified
33
Q

What is the effect of glucocorticoids?

A
  • Inhibit transcription of pro-inflammatory genes
    > Cox2, Cytokines (IL-2, TNF-a, IL-1, IL-4, ), Adhesion molecules
  • Induce expression of anti-inflammatory genes
    – Lipocortins (annexin I), IL-10, IL-1ra, soluble IL-1r
    > Lipocortin inhibit phospholypase A2; Inhibit leukocyte activities and activating lipoxin A4 receptor
34
Q

How does Nitric oxide act as a mediator of inflammation?

A

1- Vasodilation: NO can cause blood vessels to relax and dilate, leading to increased blood flow to the site of inflammation.

2- Recruitment of Immune Cells: NO can promote the recruitment and activation of immune cells, such as neutrophils and macrophages, to the site of inflammation.

3- Production of Reactive Nitrogen Species: High levels of NO can lead to the production of reactive nitrogen species (RNS)= cytotoxic and cause damage to proteins, lipids, and DNA.

35
Q

How does Adenosine act as a mediator of inflammation?

A

1- Inhibition of Immune Cell Activation
2- Suppression of Cytokine Release: Adenosine can reduce the production and release of pro-inflammatory cytokines
3- Modulation of Adhesion Molecules: Adenosine can reduce the expression of adhesion molecules on the surface of endothelial cells.
4- Promotion of Regulatory T Cells: Adenosine can promote the differentiation and function of regulatory T cells (Tregs)

36
Q

Enzymes are mediators of inflammation.
What are the functions of different complement proteins?
C3a
C5a
C3b
MAC(C3b-9

A

C3a- Increase vascular permeability
C5a- Increase vascular permeability + chemotaxis
C3b- Opsonisation
MAC(C3b-9- Cell lysis

37
Q

How is the kinin system a mediator of inflammation?

A

Tissue injury/ collagen > Cascade to produce bradykinin =

  • Bradykinin promote vasodilation + increase vascular permeability and stimulate the release of pro-inflammatory molecules
  • Stimulate nerve endings and enhance the sensation of pain (hyperalgesia).
38
Q

How is the coagulation/fibrinolytic cascade mediator of inflammation?

A
  • During Inflammation some elements of coagulation cascade are activated

Thrombin > leukocyte adhesion and fibroblast proliferation

Factor Xa/ Fibrinopeptides > Regulate vascular permeability + leukocyte exudation

Plasmin > affects complement system C3a

39
Q

1- What are Phosphorylesterases?
- How are some Phosphorylesterases mediators of inflammation?

2- Give an example

A

1- Enzyme SUPERFAMILY – play a crucial role in regulating intracellular levels of cyclic nucleotides controlling cAMP and cGMP catabolism
> PDEs hydrolyze cyclic nucleotides, terminating their signaling effects.
Normally > Elevated levels of cAMP are generally associated with anti-inflammatory effects… PDEs, by hydrolyzing cAMP, reduce its concentration and may thereby promote inflammation.

2- E.G. PDE4: mainly present in immune cells, epithelial cells and brain cells

40
Q

Cytokines promote differentiation, proliferation and activation of leukocytes.
Name the effect of the following cytokines in relation to how they mediate inflammation.

1-IL-1, TNF-a
2- IL-3
3- IL-4, INF-y
4- IL1b, IL17, TNF-a
5- IL-17
6- IL-6
7- IL-1, IL-17, IL

A

1- Promote leukocyte adherence to endothelium

2- Promote leukocyte production in bone marrow

3- Promote B-lymphocyte class switching

4- Activate local tissue destruction

5- Regulate chemokine production + induces haemotopoetic growth factors

6- Induce acute phase protein production at the liver

7- Induce vascular changes

41
Q

How are chemokine mediators of inflammation?

A
  • Attract leukocytes
42
Q

How is platelet activation critical in the development of inflammation? (5)

A

1- Blood clotting > Role in coagulation enzyme cascade

2- Immune response > cytokine + chemokine release, Activate leukocytes by contact , release ROS + MMP, induction of NET release

3- Coordinating leukocyte migration and activation > via humoural factors

4- Vascular responses, repair processes and chronicity > regulate extracellular adenosin

5- Sentinel for pathogens > TLRs and PRRs, acting as decoy, pathogen engulfment

43
Q

How are Evs important mediators of inflammation? (2)

A
  • Extracellular vesicles
    > Cell communication: carry signaling molecules, cytokines, chemokines, and other bioactive molecules from one cell to another.
    > Amplification of Inflammatory Signaling: EVs released by immune cells can contain components of inflammatory signaling pathways. When these EVs are taken up by neighboring immune cells or target cells, they can activate or amplify inflammatory responses by delivering inflammatory mediators or activating receptors on the recipient cells.
44
Q

True/False Antibodies, cells, receptors and soluble factors are mediators of inflammation?

A

YES

Unit 9 (9 decks)

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