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BVetMed - Animal Welfare > Inflammation and Immunity > Flashcards

Inflammation and Immunity Flashcards

1
Q

What is another name for glandular fever?

A

Epstein barr (virus?)

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2
Q

What are the 4 cardinal signs of inflammation?

A 
Heat (Calor)
Redness (Rubor) 
Swelling (Tumor) 
Pain (Dolor) 
- Loss of function added by Virchow 19thC ("Father of modern pathology")
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3
Q

How are the 4 cardinal signs caused during inflammation?

A

Heat - local increased blood flown systemic fever (pyrexia)
Redness - ^ blood flow, vasodilation (due to bradykinin, serotonin, histamine, NO)
Swelling - oedema, ^ vascular permeability -> loss of plasma, IG, extravasation of leukocytes
Pain - hyperaesthesia of nerves - due to PGs and bradykinin

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4
Q

What do paracetamol and aspirin act on?

A

Prostaglandins - prevent their production

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5
Q

What does tissue homeostasis consist of?

A

Constant balance of injury and healing, keeping the cell towards the healthy end of the
healthy -> diseased -> necrotic
scale

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6
Q

What are monocytes/macrophages? How may they be distinguished?

A

Sentinels of the immune system

  • Big single nucleus
  • Vesicles due to endocytosis/phagocytoisis of other materials
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7
Q

How do tissues monocytes function?

A

> Constantly ingest small amounts of environment to test for pathogens or foreign material
When activated, become phagocytic (termed macrophages) and release pro-inflamaotry cytokines (IL1, IL6, TNFa, interferons)
Mature to become part of the adaptive immune response
Become NON-phagocytic, MHC2 antigen presenting cells
Play a role in immune differentiation - instructing lymphocytes
release IL12, IL6, IL23, IL27, IL10

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8
Q

Give examples of regulatory cytokines

A

IL10, TGFb

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9
Q

Give an example of a species specific difference in leukocyte levels

A

Cows have low neutrophils - they are released rapidly form the bone marrow in response to stress

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10
Q

Where are neutrophils stored?

A

Blood and bone marrow

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11
Q

What is the role of naive neutrophils?

A

Phagocytic - contain proteases, oxidative burst potential, Cytokines IL8, FCyRIII “Stick” part of Ab.

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12
Q

What happens upon activation of neutrophils?

A 
Chemotaxins released (chemokines, cytokines, complement components, leukotrienes) 
Adhesion to endothelium, migration to tissues
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13
Q

Which pathogens are neutrophils particularly important for?

A

Bacteria

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14
Q

What are acute phase proteins? Give 5 examples.

A

Present in normal plasma, ^ synthesis by liver in response to IL1, IL6, other pro-inflam cytokines

  • Purpose not really understood! But measured for diagnostics.
    1. Serum amyloid A - recruits neutrophils, cholesterol transport, induces enzymes for ECM proteolysis
    2. Fibrinogen - blood clotting for extra-vascular matrix
    3. A-acid glycoprotein - binds basic drugs, steroids, protease inhibitors
    4. C-reactive protein - 50,000x ^ in acute infection - binds phosphocholine (lipid membrane component of microbial/cellular origin) assists complement binding, opsonises bacteria
    5. MBL (mannonse binding lectin) - activates complement
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15
Q

What are the 4 proteolytic cascades?

A
  1. Coagulation system - blood clotting (fibrinogen -> fibrin)
  2. Kinin system -
  3. Complemet system - MAC
  4. Fibrinolysis systm - Breaking down clot
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16
Q

What does the tetanus vaccine contain?

A 
Tetanus toxin (inactivated)
- Abs produced to bind to toxin
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17
Q

Does MAC formation occur only on bacterial cells?

A

Can occur on self cells - if virus infected this is adaptive, if healthy this is non adaptive

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18
Q

What is serum sickness?

A

Too many Ab/Ag complexes in the blood -> type 3 hypersensitivity reaction against animals own serum, esp. horses

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19
Q

What can initiate the MAC cascade?

A

MBL (mannose binding lectin) - sugar found in yeast/funghi
Ab/Ag complexes
Pathogen surfaces

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20
Q

What is the end result of the MAC cascade?

A

Formation of a MAC complex in the cell membrane - leads to lysis of cells due to ion and H20 infiltration

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21
Q

What are the two initial substances required for the kinin system cascade?

A

Prekallikrein and Prolylcarboxypepidase (in neutrophils and endothelium?) Factor XIIa

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22
Q

What are the outcomes of activation of the kinin cascade?

A

Bradykinin - acting on endothelial cells ^PG (-> pain) ^NO (-> vasodilation and ^permeability)

  • recruits and activates neutrophils
  • activates monocytes and causes cytokine release
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23
Q

What are the two initiating pathways of the clotting pathway? Where do the converge?

A

Extrinsic (damage to tissues outside the vessel wall) and intrinsic (damage to the vessel wall)
Both lead to activation of factor X

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24
Q

What does the clotting cascade cause?

A

Fibrinogen -> Fibrin –(FACTOR VIII)-> Blood clot

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25
Q

What initiates the intrinsic pathway? Which breeds may have problems with this?

A

Exposed collagen and von Willebrand factor

- Dobermans prone to lack von WIllebrand factor meaning cuts -> excessive bleeding

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26
Q

What is the initial substance in the fibrinloysis system? Which drugs are associated with this?

A

Plasminogen - Clot removal drugs for heart attack patients ^ plasminogen

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27
Q

What convert plasminogen to its active form?

A

TPA - tissue plasminogen activating converts plasminogen -> plasmin, which breaks down fibrin in the clot to degradable products

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28
Q

What is the process following endothelial damage?

A 
Exposed sub-endothelial collagen and von Willebrand factor recruits circulating factor VIII, collagen and vWF and PLATELETS
Platelets adhere to collagen (ATP dependent) 
Activated platelets release 
- ADP
- 5HT (^tone -> ^BP)
- PAF
- vWF
- Platelet factor 4
- TXA2 (vasoconstrictor)
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29
Q

What type of cascade are all 4 blood plasma cascade systems?

A

Proteolytic

- all have cross over links too.

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30
Q

What is the 2 component signal initially proposed to explain how the body discriminates pathogen, nonthreatening foreign antigen and self?

A
  1. Antigen - 3D B-cell epitope, linear T-cell epitope

2. PAMPS - pathogen associated molecular patterns - receptors of the innate immune system

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31
Q

Where are the majority of TLRs for PAMPs found?

A

Surface of monocytes and surface of endosome within monocytes

32
Q

Give an example of a PAMP

A

Lipopolysacharide

Flagellae

33
Q

What is the function of C-type lectin - Dectin1?

A

Responds to fungal sugars

  • monocytes, induces oxidative burst, IL10, CXCL2
  • dendritic cells, stimulates maturation, IL6, IL23
34
Q

Give examples of PRRs

A

MAC
NOD like receptors in the cytoplasm
- assemble into an inflammasome, activating IL1 and enabling its release

35
Q

What is gout caused by? What can exacerbate it?

A

Urate crystals due to lack of enzyme (metabolic disorder)

  • ATP/ADP levels trigger it
  • ^protein exaccerbates due to ^ urate production
36
Q

When may reactive oxygen species be produced?

A

Frustrated phagocytosis of large particles eg. silica, irate, parasites
Neutrophils stimulate monocytes to produce these
ROSs -> inflammasome assembly

37
Q

What patterns are seen in cases of sterile inflammation?

A

Damage Associated Molecular Patterns

38
Q

What may cause sterile inflammation?

A

Monosodium urate, calcium pyrophosphate, alumn crystals (eg. vaccines -> good Ab response), Asbestos

39
Q

What are the 4 mechanisms of pyrexia formation?

A
  1. Production of endogenous pyrogens (Interferon, TNFa)
  2. Binding to poiod receptors on nerve cells in hypothalamus
  3. Activation of COX2 in hypothalamus -> ^PGE2
  4. Altered firing rate of temperature sensitive neurone in anterior hypothalamus
40
Q

Outline sickness behaviour

A

Motivational state responsible for re-organising perceptions and action to enable ill individuals to cope better with infection

  • v motility
  • social withdrawal, reduced responsiveness
  • reduced food/water intake
  • ^ slow wave sleep
  • altered cognition
  • ^pain sensitivity

> mediated by effects of pro-inflammatory cytokines (esp IL1) on CNS
IL1, IL6, TNF, interferon released in response to PAMPs

41
Q

What is inflammation?

A

A conserved response of living tissues to external threats or damage - the first step in healing of diseased or injured tissue

42
Q

Which stimuli can cause inflammation?

A

Many - infection, toxins, physical agents, products released from dead or dying cells (STERILE INFLAMMATION)

43
Q

Why should unregulated inflammatory response be kept in check?

A

Can cause further tissue damage

44
Q

What is the action of B cells? Where are they stored?

A

Secrete antibodies

Follicles in the lymph nodes

45
Q

What is the purpose of antibodies?

A

Recognise 3D shapes by the epitope

Multiple binding sites enables complex formation (agglutination)

46
Q

What do T cells recognise?

A

Short peptide segments on antigen presenting cells

47
Q

What are the 2 main subgroups of T cell? What is their function and where are they found?

A

CD4+ Helper T cells - make cytokines, activate and control immune responses - EXTRACELLULAR
CD8+ Killer T celler - make cytotoxic substances swell as cytokines - INTRACELLULAR

48
Q

What type of MHC do each of the T cells interact with?

A

CD8 - MHCI

CD4 - MHCII

49
Q

What is the MHC:T cell junction referred to as?

A

Immunological synapse

50
Q

What does MHCII antigen presentation lead to?

A
  • activated CD4 helper cells
  • helper cells secrete cytokines to direct immune response
  • Activate NK cells (innate virus response)
  • Help expansion of cytotoxic T cells
  • Help B bell antibody production
  • Essential for immune memory
51
Q

What does B cell antibody class switching require?

A

T cell help via cytokines

52
Q

Which section of antibody binds antigens?

A

Variable light chain

Other section is the constant heavy chain.

53
Q

Which section of the antibody changes in class switching?

A

Heavy “constant” chain

54
Q

Which order does class switching occur?

A

MDG(bacteria)A(mucosal)E(parasite/allergy)

55
Q

Do all species have the same number of Ab classes?

A

No - eg. horses have 7

56
Q

How may antibodies be antibacterial?

A
  • recognise unique proteins and polysaccharides
  • prevent adhesion and invasion
  • opsonise bacteria ready for phagocytosis
  • activate complement
    > specific antibodies may neutralise secreted toxins eg. tetanus
57
Q

What responds to PAMPs?

A

PRRs - patterns recognition receptors

58
Q

What are tissue macrophages (from monocytes) activated by?

A

TLR (toll like receptor) activation

59
Q

What are the properties of an activated macrophage?

A 
^ innate antimicrobial function 
- enhanced phagocytosis
- enhanced production of ROS 
- enhanced NO production 
- enhanced phagosome lysosome fusion 
^adaptive immune function 
- ^ MHC expression for antigen presentation 
- ^ interferon production 
- ^ cytokine/chemokine productino
60
Q

How do neutrophils destroy pathogens?

A

Oxidative burst - NAPDH oxidase, superoxide dismutase and myeloperoxidase involved int he reaction

61
Q

Which subsection of complement inserts into the cell membrane?

A

C3a

62
Q

How long to macrophages/dendritic cells live?

A

Long time

63
Q

How do macrophages migrate around the body?

A

Blood and lymph

64
Q

How do macrophages destroy pathogens?

A

Phagocytosis/Pinocytosis - WEAK oxidative burst

65
Q

How are macrophages involved in the adaptive immune response?

A

Antigen Presentation

66
Q

How long to neutrophils live?

A

Short life span

67
Q

Where are neutrophils stored?

A

Bone marrow/blood

68
Q

What happens to neutrophils following initiation of an inflammatory response?

A

Rapid migration to tissue at inflamed sites - cannot recirculate
- potent oxidative killers following phagocytosis of pathogens

69
Q

Which cells and cytokines are involved in virus immune response?

A

NK cells and T cells - Interferon Gamma
Epithlium releases Interferon b to alert surrounding cells
Fibroblasts release interferon b
Macrophages/plasmacytoid dendritic cells - Interferon a, IL1, IL6

70
Q

What do interferons do?

A

Alert neighbouring cells to virus infection via receptors -> genetic changes ^ resistance to viruses

  • Degrade RNA in RNA viruses
  • Block protein production
  • ^ expression of MHC
  • Activate immune cells and NK cells
  • Mediate fever response and sickness behaviour
71
Q

What are respiratory viruses particularly good at?

A

Blocking interferon communication between cells

Also surviving at lower temperatures

72
Q

What do NK cells monitor?

A

Production of MHC - if MHC production v -> apoptosis

73
Q

What activates NK cells and what do they produce?

A

Interferon gamma (IFNy) and IFNy!

74
Q

How may antibodies protect from viruses?

A

Bind to agglutination receptors and prevent binding onto cell surfaces (and thus prevent entry into the cell)
Initiate MAC formation in the infected cell -> apopotosis

75
Q

Which cells express MHCI? What is it’s action?

A

ALL cells

  • highest concentration on leukocytetes
  • Interferon ^ expression of MHCI
  • Presence of MHCI Inhibits NK cell killing
  • Presents antigen to CD8 killer cells
  • Healthy cels will present self antigen in the peptide groove, whereas infected cells may present foreign antigen
76
Q

How do CD8+ T cells respond to MHCI?

A

If foreign peptide is presented will destroy cell so that virus infected cells cannot reproduce
- ^no of CD8 memory cells protect from reinfection

77
Q

What is another method of destroying virus infected cells?

A

CASPASE cascade

Perforin and granzymes

BVetMed - Animal Welfare (19 decks)

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