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Clinical Immunology and Haematology > Inflammation and Recruitment of Inflammatory Cells > Flashcards

Inflammation and Recruitment of Inflammatory Cells Flashcards

1
Q

What are the 5 cardinal signs of inflammation and how are these caused?

A

Redness - causes by vasodilation and increased blood flow
Heat - caused by vasodilation and increased blood flow
Swelling - Accumulation of fluid
Pain - irritation of nerve endings
Loss of Function - destruction of tissue or to avoid pain

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2
Q

Why does inflammation occur?

A

As a response to a threat

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3
Q

What cells are involved in the inflammatory response?

A

Innate and accute cells

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4
Q

What would happen if you got pricked with a bacteria covered pin?

A

Chemical signals are generated by resident cells and leukocytes from the blood are recruited to these signals (mainly phagocytes/neutrophils). These digest and kill the pathogen and inflammation is resolved.

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5
Q

What are the inflammatory cells?

A

Leukocytes - Neutrophils, Eosinophils, Mast cells, Basophils, T-cells, NK cells and platelets.

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6
Q

What is the function of inflammation?

A

Host defence agaisnt micro-organisms - this can be sterile or infectious.

Control of tumour growth and mestasis

Tissue repair and restoration of organ function

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7
Q

The stages of acute inflammatory response?

A

The pro-inflammatory response

Anti-inflammatory and pro resolution response

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8
Q

What does the pro-inflammatory response involve?

A

The pro-inflammatory response to kill and remove pathogens. This involves inflammatory cell recruitment and indentification of the insults.

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9
Q

What does the anti-inflammatory and pro-resolution response involve?

A

Inflammatory cell phenotypic change, removal of recruited inflammatory cells and repair of damaged tissue.

This is all to return the tissue back to homeostasis.

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10
Q

How does the body identify the insult?

A

All invasions give of signals - either pathogen associated molecular patterns (PAMPs) or damage associated molecular patterns (DAMPs aka alarmins).

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11
Q

What are examples of PAMPs?

A

Carbohydrates, lipids, proteins, nucleic acids

Anything that you would not see in your body

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12
Q

What are examples of DAMPs?

A

Mitochondrial components, nuclear protiens, stess-induced proteins, crystals.

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13
Q

What notices these PAMPs/DAMPs?

A

Pattern recognition receptors (PRRs)

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14
Q

Examples of Pattern recognition receptors?

A

Toll like receptors,
NOD-like receptors
C-type lectin receptors
FPRs

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15
Q

Can pattern recognition receptors be membrane bound or cytosolic?

A

Yes

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16
Q

What do Toll-like receptors recognise?

A

Microbes and molecules released by stressed/dying cells

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17
Q

What do TLRs differ in?

A

Membrane localisation and ligands recognised

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18
Q

What does ligation of a TLR do?

A

Induces signal transduction cascade (e.g. cytokines) that ultimately regulates expression of inflammatory genes.

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19
Q

What do NRS do?

A

They are intracellular receptors which apon ligation induce an inflammatory response by facilitating the activation of caspase-1, resulting in processing or pro-cytokines and releasing mature cytokines.

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20
Q

What type of cell death are NLRs involved in?

A

Pyroptosis

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21
Q

What do NLR’s create?

A

Inflammasomes

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22
Q

What are some types of inflammatory mediators to regulate cellular functions?

A

-Vasoactive amines e.g. histone, seratonin
-Complement components e.g. C3a and C5a
-Lipid mediators e.g. prostaglandins, leukotrienes and platelet activating factor
-Cytokines and chemokine e..g TNF, IL-1, IL-6, IL-8 etc.

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23
Q

What is the leukocyte adhesion cascade?

A

Leukocytes role along the endothelial wall and are slowed down by E-selectin. They are then stopped by activated integrins. The leukocyte is then polarised and transmigration occurs (the leukocyte goes through the tissue) to follow the chemokine trail to infection.

24
Q

What causes leukocytes to roll along the endothelial wall?

A

Selectins control tethering and rolling

25
Q

How do selectins control bidning and rolling of leukocytes?

A

By binding to the carbohydrate ligands - glycoproteins and glycolipids (L-selecting, P-selectin and E-selectin)

26
Q

What does the L-selectin do?

A

Its expressed by leukocytes, mediates capture and is shed following activation.

27
Q

What does P-selectin do?

A

Its expressed by endothelial cells anf platelets to mediate rolling

28
Q

What do E-selectins do?

A

Expressed by activated endothelium (cytokine-induced), mediates slow rolling

29
Q

What signals do integrins need to stop the rolling leukocyte along the endothelial wall?

A

Selectin and chemokine signals

30
Q

When and why are chemokines immobilised?

A

They are immobilies on the endothelium so they can be presented to circulating leukocytes.

31
Q

Chemokine receptors - what happens after ligation?

A

Activation of the rolling neutrophil bu immobilised chemokines causes selectin shedding and LFA-1 integrin activation.

32
Q

What does integrin activation by chemokines enable?

A

Firm leukocytes adhesion to the vessel wall

33
Q

What do integrins bridge?

A

Extracellular ligans and actin cytoskeleton.

34
Q

Where are integrin ligands displayed?

A

On the endothelium

35
Q

What two positions can ligands have and why would they change positions?

A

Bent (low affinity)
Extended (high affinity - active and can bind ligand)

Regulated by activation based on chemokines.

36
Q

What integrin binds the ligand?

A

LFA-1 and this only occurs after a selectin and chemokine activates it.

37
Q

What is the ligand integrin binds to on the leukocyte?

A

ICAM-1

38
Q

When is ICAM-1 upregulated on endothelial cells and leukocytes?

A

Cytokine stimulation

39
Q

What are the two modes of transendothelial migration (through the endothelium)?

A

Paracellular or transcellular

40
Q

In vivo what is the main pathway of transendothelial migration?

A

Paracellular

41
Q

What is leukocyte adhesion deficiency?

A

Deficiency in Beta2 integrins characterised bu frequent bacterial disease and is often fatal.

42
Q

How do you remove a threat.

A
43
Q

How do you remove a threat - what do chemokines and chemoattractants do?

A

Direct leukocyte chemotaxis towards site of inflammation once endothelial barrier has been breached.

44
Q

How are pathogens killed after following chemoattractants?

A

Internally following engulfing

45
Q

Is apoptosis a pro-resolution type of cell death?

A

Yes

46
Q

Is necrosis a pro-resolution type of cell death?

A

No - it shows the immune system the antigen to encourage immune response.

47
Q

What does killing of phagocytosed microbes initiate?

A

Pro-resolution signals

48
Q

How does the phagocyte clear apoptotic cells?

A

Through efferocytosis

49
Q

How does efferocytosis occur?

A

The apoptotic neutrophil generates find me signals causing the macrophage to come over. They ingest the neutrophil and this causes the macrophage to become anti-inflammatory.

50
Q

What signals do anti-inflammatory signals produce?

A

Pro-resolving lipids,
Anti-inflammatory cytokines

51
Q

Why wouldn’t you be able to resolve inflammation?

A

Inadequate production of resolution mediators, prolonged or excessive response, persistant stimulation, subnormal response, infiltration by myeloid-derived supressor cells and failed phenotypic switch in macrophage and T cell populations.

52
Q

What are some diseases coming from non-resolved inflammation?

A

Atherscierosis, COPD, cancer, obesity, asthma, IBD, RA, MS

53
Q

What are inflammatory disease?

A

Inappropriate host response leading to disease which can affect virtually every organ in the body.

54
Q

What is gout?

A

A common type of arthritis causing painful flare-ups, often in the big toe driven by a build up of uric acid crystals active inflammasome.

55
Q

How do you treat gout?

A

IL-1b therapy

56
Q

How would you therapeutically target inflammation?

A

Small molecule inhibitors
Antibody-mediated
Use of soluble decoy receptors

Clinical Immunology and Haematology (25 decks)

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