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MMI 436 > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What is acute inflammation characterized by?

A

Movement of serum proteins and leukocutes (esp granulocytes - neutrophils, eos, baso.) from the blood –> extravascular compartments

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2
Q

Describe the vascular and cellular phase of inflammation

A
  • vascular phase: vessel dialation and increased permeability promotes the movement of plasma and proteins (e.g. fibrin, Abs)
  • cellular phase: chemotactic mediators and endothelial cell activation recruit immune cells (esp granulocytes) through extravasation
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3
Q

What are the five signs of inflammation? Include latin term

A
  1. calor (heat)
  2. rubor (redness)
  3. tumor (swelling)
  4. dolor (pain)
  5. functio laesa (LOF)
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4
Q

For both acute and chronic inflammation:

  • definition
  • when does the response first appear
  • how long does it last
  • which cells are involved
A

acute:

  • definition: limited tissue response that starts immediately after injury
  • onset: immediate
  • duration: several days - IT RESOLVES
  • cells: 1st - innate immune cells (PMNs); 2nd - lymphocytes

chronic:

  • definition: prolonged response
  • onset: delayed onset
  • duration: months to years
  • cells: lymphocytes, MFs, and plasma cells (adaptive IS is the primary driver of acute inflammation)
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5
Q

What initiates inflammation?

A

PAMPS and DAMPS

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6
Q

Describe NF-kB activation

A
  1. IKK complex phosphorylates NF-kB:IkB
  2. NF-kB:IkB-P is ubiquitulated and IkB is degraded in the proteosome
  3. NF-kB translocates to the nucleus
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7
Q

What defines the TLR/IL-1 superfamily?

A

TIR domain

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8
Q

For the following PAMPs, what TLR do they activate, and where is that TLR located:

  • LPS
  • flagellin
  • dsRNA
  • ssRNA
  • CpG DNA
A
  • LPS –> TLR4 (pm)
  • flagellin –> TLR5 (pm)
  • dsRNA –> TLR3 (endosome memb)
  • ssRNA –> TLR 7/8 (endosome memb)
  • CpG DNA –> TLR 9 (endosome memb)
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9
Q

Describe the MyD88 and TRIF signaling pathways of activated TLRs

A

MyD88 –> TRAF 6 –> TAK 1 –> NF-kB –> proinflammatory cytokines

TRIF –> TRAF 6 –> etc

TRIF –> TRAF 3 –> IRF3 –> type 1 IFNs

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10
Q

What are NLRs? What are the two subfamilies, give examples for each subfamily

A

NLRs = intracellular sensors of PAMPs that enter the cell via phagocytosis or pores, and DAMPs associated with cell stress

Subfamilies
1. NLRC: NOD1/2, NLRC3/4/5
2. inflammasomes: NLRP3

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11
Q

Describe the formation of the inflammasome and its function

A

formation: PYD of NLRs binds to adapter protein ASC (PYCARD) via PYD-PYD interaction –> ASC links NLRs to inactive form of caspase 1 via the CARD domain

function: aggregation of pro-caspase 1 –> autocleavage to active caspase 1 –> caspase 1 cleaves pro-IL-1B to IL-B1 (inflammatory cytokine) + activates pore proteins –> cytokine release (creates the ILs and opens the door)

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12
Q

What are RLRs? Give a couple examples of RLRs and what they activate.

A

RLRs = family of cytoplasmic PRRs that sense RNA, provide frontline defense against viral infections in most tissues

e.g. RIG-I and MDA5 –> activate NF-kB

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13
Q

what are CLRs? give examples of DC and MF CLRs and their functions

A

CLRs = carbohydrate-binding lectins, require Ca2+ for binding

examples:
* CLECs
* MMR –> scavenger R
* DEC-205 –> cross presentation
* dectins –> fungi detection
* langerin –> specific of Langernans cells

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14
Q

What are KLRs?

A

NK cell lectin-like Rs: both activating and inhibitory types

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15
Q

DAMPs

For the following DAMPs, state their intracellular location and their receptors:
* genomic DNA
* HMGB1
* ATP
* uric acid crystal

A
  • genomic DNA: nucleus, TLR9
  • HMGB1: nucleus, TLR2/4, RAGE
  • ATP: cytosol, P2Y2, P2X7
  • uric acid crystals: cytosol, NLRP3
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16
Q

For the following mediators of inflammation categories, describe the mediators, main sources, and primary functions:

  • vasoactive amines
  • vasoactive peptides
  • proteolytic enzymes
A

vasoactive amines:

  • histamine from mast cells and basophils –> vasodilation, increases permeability
  • serotonin from platlets –> vasodilation, increases permeabiltiy

vasoactive peptides:

  • Kinins from plasma –> vasodilation, increases permeability

Proteolytic enzymes

  • serine proteases from plasma –> leukocyte recruitment
  • nonserine proteases (e.g. MMPs) from plasma and leukocytes –> tissue remodelling
17
Q

Name and describe four groups of lipid mediators (eicosanoids)

A
  1. prostaglandins: vasodilation, increase permeability, fever, pain, eosinophil and mast cell recruitment
  2. thromboxane: vasoconstriction and platelet aggregation
  3. Leukotrienes: LTB4 - chemoattractant and activator, adhesion of WBCs
  4. cysteniyl LT: vasoconstricion, increased permeability, bronchoconstriction, mucus secreation (anaphalaxis)
18
Q

Describe the formation of prostaglandins, thromboxane, and leukotrienes

A

prostaglandins and thromboxane: phospholipids –> arachidonic acid (AA) –> COX pathway –> prostaglandins and thromboxane

leukotrienes: phospholipids –> AA –> LOX –> leukotrienes

19
Q

What are the three complement pathways? Briefly describe each

A
  1. classical: C1q interacts with Abs bound to surface of pathogens
  2. lectin: ficoline and MBL (CLRs) bind carbohydrates on pathogen surface
  3. alternative: C3 undergoes spontaenous hydrolysis - factor B binds C3 and is cleaved by factor D
20
Q

Describe the complement cascade for all three pathways

A

classical: Ag-Ab complex + C1, C4, C2 –> C3 convertase (C3 –> C3b) –> C5 convertase (C5 –> C5b) –> C5b, C6, C7, C8, C9 –> MAC

alternative: activating surfaces (e.g. LPS) –> C3b + factor B –> C3 convertase –> etc

lectin: C4, C2, MBL –> C3 convertase –> etc

21
Q

What are 6 functions of the complement?

A
  1. promote inflammaiton
  2. opsonization
  3. B cell activation and differentiation
  4. cell lysis (MAC)
  5. immune cell complex clearance
  6. apoptotic cell removal
22
Q

Describe the JAK-STAT signaling pathway

A

cytokine binds to cytokine R which contains JAK (kinase) –> dimerization –> JAKs phosphorylate the Rs –> STATs (TFs) bind to phosphorylated Rs using their SH2 domain –> STATs are phosphorylated and activated by JAKs –> STATs dimerize and translocate to the nucleus

23
Q

Describe Smad signaling

A

cytokine binds to R –> crosslinkage –> phosphorylation of R –> activated R phosphorylates R-Smad –> R-Smad-P:R-Smad-P:Smad4 translocate to nucleus

24
Q

When endothelial cells are activated, what are the four core changes?

A
  1. loss of vascular integrity (opening of tight junctions)
  2. expression of leukocyte adhesion molecules (integrins and CLRs)
  3. change in phenotype from antithrombotic –> prothrombotic
  4. inflammatory mediator production
25
Q

What are the 4 subfamilies of chemokines? What type of Rs do chemokines bind to?

A

subfamilies:
1. C
2. CC
3. CXC
4. CX3C

interact with G protein-linked transmembrane Rs

26
Q

Describe G protein signaling (only include important factors)

A

activated GCPR –> GyGB –> PIP2 –> rho family GTPases –> effectors –> adhesion, contraction, F-actin polymerization

27
Q

For the following chemokine Rs, describe which cells they’re found on:

  • CXCR1/2
  • CXCR3
  • CCR2
  • CCR3
A
  • CXCR1/2 –> neutrophils
  • CXCR3 –> Th1
  • CCR2 –> monocytes
  • CCR3 –> eos, basophils
28
Q

Describe leukocyte extravasation

A
  1. endothelial activation
  2. tethering and rolling
  3. chemokine presentation –> integrin activation (integrin goes from inactivated/closed –> active/open conformation) on leukocytes and endothelial cells
  4. slow rolling and arrest
  5. firm adhesion and intraluminal crawling
  6. transendothelial migration/diapedesis (paracellular - between cells; transcellular - through a cell)
  7. sub-endothelial crawling

MMI 436 (14 decks)

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