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Immunology - CORE > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What are the symptoms of acute inflammation?

A
  • swelling and redness
  • heat and fever
  • pain
  • loss of function
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2
Q

What are the major cell mediators of acute inflammation and what do they secrete?

A
  • neutrophils - TNF-α
  • macrophages - IL-6
  • mast cells - IL-1
  • endothelial cells - acute phase proteins
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3
Q

Describe prostaglandins and inflammation

A
  • PGE2 can sensitise nerves to pain
  • PGE2, PGE1 and others involved in vasodilation
  • PGE2 involved in fever with IL-1
  • production of PG is mechanism of action for NSAIDS
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4
Q

Describe PAMP/PRR in acute inflammation recognition

A
  • innate cell recognition of pathogens
  • macrophages and neutrophils
  • also mast cells - not just Th2/IgE response
  • TLRs and other PRRs also important
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5
Q

Describe DAMPs in acute inflammation recognition

A
  • innate cell recognition of damage
  • host proteins
  • nuclear and cytosolic proteins usually hidden
  • therefore innate immune system should only see when necrosis has occured
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6
Q

Describe DAMPs

A
  • damage associated molecular patterns
  • chromatin-associated protein high-mobility group box 1: HMGB1 - TLR4
  • head shock proteins TLR-4
  • DNA - TLR9
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7
Q

Describe the released mediators in acute inflammation

A
  • activation of neutrophils, macrophages and mast cells
  • secondary responses by endothelial cells
  • releases TNF-α, IL-1, IL-6, Histamine and Chemokines CCL2, CCL5, CXCL8
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8
Q

What causes redness and heat in acute inflammation?

A
  • IL-1 and TNF-α
  • leads to vasodilation and vascular permeability
  • capillaries closer to surface
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9
Q

What causes swelling in acute inflammation?

A
  • chemokines
  • cellular infiltration at site of infection/damage
  • upreg of adhesion molecules on endothelia (IL-1)
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10
Q

Describe the acute phase response

A
  • pro-inflammatory cytokines (mainly IL-6) lead to upreg & downreg of proteins
  • release of acute-phase proteins in liver
  • opsonisation
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11
Q

Describe the release of acute-phase proteins from liver in acute phase response

A
  • haptoglobin
  • fibrinogen
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12
Q

Describe haptoglobin

A
  • increased in horses, cattle, rabbits, sheep, humans
  • binds haemoglobin
  • prevents bacteria requiring iron from gaining it
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13
Q

Describe fibrinogen

A
  • increased in horses, rabbits, humans
  • potential damage to tissues
  • cleavage of fibrinogen to generate fibrin threads
  • clot can block pathogen
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14
Q

Describe opsonisation

A
  • mannan-binding lectin
  • c-reactive protein
  • complement
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15
Q

Describe complement in opsonisation

A
  • C3a - mast cell activation/degranulation
  • C4a - mast cell activation
  • C5a - chemotaxis, vasodilation, neutrophil & mast cell activation/degranulation
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16
Q

What causes pain in acute inflammation?

A
  • damaged endothelial cells and platelets produce pain response mediators - seratonin
  • plasma leaking from blood vessels contains bradykinin
  • seratonin and bradykinin stimulate nerve endings
17
Q

What are some diseases associated with inflammation?

A
  • sepsis
  • toxic shock syndrome
  • cytokine storm
18
Q

Describe sepsis

A
  • range of bacteria causes
  • macrophages and DCs activated by bacteria
  • overproduction of IL-1 and TNF-α
  • increased blood vessel permeability, decreased blood pressure
  • local and systemic effects of cytokines IL-1, IL-6 and TNF-α induce clinical symptoms associated with septic shock
19
Q

Describe toxic shock syndrome

A
  • caused by bacterial protein toxins: enterotoxin type B or TSST-1 or Spe1 and SpeC
  • known as superantigens:
  • bind to MHC class II and TCRs
  • activates 5% of T cells - normally 0.01%
  • production of TNF-α and IL-1
20
Q

Describe cytokine storm

A
  • hypersecretion of cytokines - positive feedback loop
  • TNF-α, IL-1, chemokines etc
  • Ebola, SARS
21
Q

Describe chronic inflammation

A
  • not only innate cells
  • T cells important
  • can be Th1, Th2, Th17
  • caused by pathogens and non-pathogens
22
Q

Describe resolution of inflammation

A
  • Tregs and Macrophages have a role
  • short half-life of inflammatory mediators
  • production of pro-inflammatory prostaglandin and chemokines stops
  • stops neutrophils migrating to site
  • existing apoptotic neutrophils phagocytosed by macrophages
  • major change in cell types
23
Q

Describe Tregs and resolution of inflammation

A
  • CD4+ T Cells producing anti-inflammatory cytokines are critical
  • secrete IL-10 and/or TGF-β
  • leads to downregulation of: Th1 production, MHC class II expression, co-stimulatory molecules
24
Q

Describe macrophages and resolution

A
  • M1 converts to M2
  • M1 Th1 associated - IL-12
  • M2 Th2 associated - IL-10, TGF-β, protease inhibitors
  • balance of M1/M2 important in helminth infections, cancers, arthritis

Immunology - CORE (18 decks)

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