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Inflamm Flashcards

1
Q

What are the 4 cardinals signs of inflammation?

A

redness
swelling
heat
pain
+/- loss of fct

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2
Q

What are the sensors of cell damage?

A
  1. TLR (DAMPs, PAMPs)
  2. Cytosolic-R = NLR (uric acid = DNA breakdown, ATP = damage mito, reduced K+, DNA)
  3. Leucocytes express R for Fc tails of AC and for complements = recognize opsonized microbes
  4. Mannose-binding lectin = recognize microbial sugars = active complement
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3
Q

How is contraction of endothelial cells elicited?

A

By histamine, bradykinin, leukotriene
15-30 min = transitoire

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4
Q

How do leucocytes get out of vessels?

A
  1. Paracellular transport 2n retraction of endo cells (histamine, NO)
  2. Transcytosis in venules upregulated by VEGF = important to cross blood-brain-barrier
  3. Endothelial injury
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5
Q

What is the immediate transient response in acute inflammation? mediation?

A

Contraction of endothelial cells that increase permeability
Mediated by histamine (pre-formed really to be released at any time)

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6
Q

The cytoskeletal reorganisation permitting transcellular leakage is mediated by :

A

IL1, IL6, TNFa

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7
Q

Steps involved in margination of leucocytes

A
  1. Microbes in tissue
  2. Tissue resident macrophages bind PAMPs/DAMPs -> release IL1, IL6, TNFs -> activate endothelial cells
  3. Activated endothelial cells upregulate preformed P-selectin (later E- L-selectin) = ROLLING
  4. Selectins binds glycosylated molecules (PSGL-1, Sialyl-Lewis X) for transient low affinity binding -> Hausse affinity for integrins
  5. Integrin high affinity state (ICAM-1) = stable adhesion
  6. Migration through endothelium via CD31 (PECAM-1)
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8
Q

Where are P-selectin stored?

A

Exists preformed in Weibel-Palade body

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9
Q

What binds to L-selectin?

A

Receptor for leucocytes extravasation
1. GlyCAM-1 = high endothelial venules in lymphoid tissue
only binds selectin
2. MadCAM = expressed on MALT in TGI
also binds integrins (VLA4, a4B7)
3. CD34 = endothelial cells

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10
Q

The expression of selectin is mediated by

A

TNF, IL1, chemokine
Histamine, thrombin stimulate P-selectin

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11
Q

Molecules involved in migration

A

CD31, PECAM1

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12
Q

How do leucocytes pierce basement membrane?

A

By secreting collagenase

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13
Q

What are exogenous chemoattractants?

A

Bacterial producst = peptide with N-terminal, aa, lipids

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14
Q

What are endogenous chemoattractants?

A

Cytokine = IL8
Complement = C5a
Arachidonic acid (AA) metabolits = leukotriene B4

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15
Q

What allows leucocytes to move following binding of chemotactic agents to GPCR?

A

extension of flipodia
actin = leading edge
myosine = back of leucocytes

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16
Q

Steps of phagocytosis

A
  1. recognition
  2. engulfment
  3. killing and degradation
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17
Q

Properties of neutrophils
1. Origin
2. lifespan in tissue
3. response
4. ROS
5. NO
6. Degranulation
7. Cytokine production
8. NET
9. Enzymes lysosomal

A
  1. Origin = HSC in bone marrow
  2. lifespan in tissue = days
  3. response = short, fast
  4. ROS = rapidly induced by phagocyte oxidase
  5. NO = low or none
  6. Degranulation = major
  7. Cytokine production = low or none
  8. NET = rapide
  9. Enzymes lysosomal =prominent
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18
Q

Properties of macrophages
1. Origin = HSC in bone marrow, tissue-resident
2. lifespan in tissue = BM = days or week, tissue-resident = years
3. response = prolonged, slower
4. ROS = less prominent
5. NO = induced after transcriptional activation of iNOS
6. Degranulation = not prominent
7. Cytokine production = major
8. NET = no
9. Enzymes lysosomal = less

A
  1. Origin
  2. lifespan in tissue
  3. response
  4. ROS
  5. NO
  6. Degranulation
  7. Cytokine production
  8. NET
  9. Enzymes lysosomal
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19
Q

Elements allowing destruction of microbes in phagocytes

A

O2, H2O2 + azurophilic granules(MPO) -> HOCl = halogenation (hyalide bound) or oxidation (lipids peroxydation)
In macrophage, NO interacts with O2 = ONOO-

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20
Q

Neutrophils granules

A

Small = lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator, histaminase, alkaline phosphatase
Larger azurophil = MPO, defensin, acid hydrolase, neutral protease

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21
Q

Macrophages content

A

acid hydrolase
collagenase
elastase
phospholipase
plasminogen activator

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22
Q

Action of a1-antitrypsin on neutrophils

A

major inhibitor of neutrophils elastase

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23
Q

NET formation

A

ROS-dependant activation of arginine deaminase converts arginine to citrulline = chromatin decondensation

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24
Q

What is frustrated phagocytosis?

A

inability to ingest (immune complex deposit on large surface) = triggers activation/release of lysosomal enzyme EC

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25
Q

How do LT contribute to acute inflammation?

A

produce IL17 inducinf secretion of chemokines to recruit leucocytes

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26
Q

What are the termination mechanisms of acute inflammation?

A

Termination begins by switching the type of AA metabolite to antiinflammatory lipoxins = liberation of antiinflamm cytokines TGFB and IL10

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27
Q

Principal mediators of inflammation source and action :
1. Histamine
2. Prostaglandine
3. Leukotriene
4. Cytokines (TNF, IL1, IL6)
5. Chemokines
6. PAF
7. Complement
8. Kinins

A
  1. Histamine
    Mast cell, basophils, platelets
    VasoD, permeability, endo activation
  2. Prostaglandine
    Mast cells, leukocytes
    VasoD, pain, fever
  3. Leukotriene
    Mast cells, leukocytes
    Permeability, chemotaxis, leuco adhesion/activation
  4. Cytokines (TNF, IL1, IL6)
    macro, masto, endocells
    endo activation, fever, metabolism, shock hypotensive
  5. Chemokines
    leuco activated macro
    chemotaxis, leuco activation
  6. PAF
    leucocytes, masto
    vasoD, permeability, leuco adhesion, chemotaxis, degranulation, oxidative burst
  7. Complement
    plasma (produced by liver)
    leuco chemotaxis/activation, MAC, vasoD
  8. Kinins
    plasma (produced by liver)
    permeability, smooth muscle contraction, vasoD, pain
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28
Q

When is histamin released?

A

Stored preformed in cells
physical injury
binding of IgE on AC of mastocytes
products of C3a, C5a
substance P, IL1, IL18 can cause release

29
Q

Where is serotonin present?

A

platelets and neuroendocrine cells (GI)

30
Q

AA derived mediators (eicosanoids) binds to what?

A

GPCR

31
Q

Action of AA metabolites :
1. PGI2, PGE1, PGE2, PGD2
2. TxA2, LTC4, D4, E4
3. LT C4, D4, E4
4. LT B4, HETE

A
  1. PGI2, PGE1, PGE2, PGD2 = vasoD
  2. TxA2, LTC4, D4, E4 = vasoC
  3. LT C4, D4, E4 = increase permeability
  4. LT B4, HETE = chemotaxis, leucocyte adhesion
32
Q

Why is COX-2 selectif inhibitor and interesting option?

A

Because COX2 generate PG involve only in inflamm rx vs COX1 involved in inflamm and physiologic protective effect
But inhibing COX2 can predispose to thrombosis

33
Q

Source and actions of cytokines in acute inflammation :
1. TNF
2. IL1
3. IL6
4. Chemokines
5. IL17

A
  1. TNF
    macro, masto, LT
    stimule expression of endo adhesion and secretion of other cytokines
  2. IL1
    macro, endo cells, epi cells
    similar to TNF, role in fever
  3. IL6
    macro and other cells
    systemic effects
  4. Chemokines
    macro, endo cells, LT, masto
    recruit other leucocytes, migration
  5. IL17
    LT
    recruits neutro and monocytes
34
Q

Source and actions of cytokines in chronic inflammation :
1. IL12
2. IFNy
3. IL17

A
  1. IL12
    DC, macro
    increase production of IFNy
  2. IFNy
    LT, NK cells
    active macro
  3. IL17
    LT
    recruits neutro and monocytes
35
Q

Role and production of tumor necrosis factor (TNF)

A

Production of TNF signals by TLR and IL1
Roles :
- endo activation (adhesion, mediators)
- activation of leucocytes, IL1
- supress appetit (cachexia)

36
Q

Role of C-X-C chemokines

A

act on neutro, IL8
secreted by macro, endo cells
inducers = microbial products, IL1, TNF

37
Q

C-C chemokines (MCP-1, CCL2, CCL11, MIP-1, CCL3) role

A

attract monocytes, eosino, baso, lympho

38
Q

C chemokines (lymphotactin, XCL1) role

A

relatively Sp for lympho

39
Q

CX3C chemokines (CX3CL1) role

A

1 - cell surface bound on endo cells = promot adhesion of monocytes and LT
2- soluble form = potent chemoattractant

40
Q

By what are triggered the 3 pathways of the complement system?

A
  1. Classical pathway = by binding C1 to IgM or IgG
  2. Alternative pathway = by microbial surface molecules
  3. Lectin pathway = plasma mannose-binding lectin binds carbohydrates on microbes = active C1
41
Q

Role of DAF, factor H and CD59

A

DAF = prevent formation of C3 convertase
CD59 = inhibit formation of MAC
Factor H = promote cleavage and destruction of C3b = inhibits alternative pathway

42
Q

Mediators of :
1. VasoD
2. Permeability
3. Chemotaxis/recruitment/activation
4. Fever
5. Pain
6. Tissue damage

A
  1. VasoD = histamine, prostaglandine
  2. Permeability = histamine, serotonin, C3a, C5a, LTC4,D4,E4
  3. Chemotaxis/recruitment/activation = TNF, IL1, C3a, C5a, LTB4
  4. Fever = IL1, TNF, PG
  5. Pain = PG, Bradykinin, substance P
  6. Tissue damage = lysosomal enzyme, ROS
43
Q

Events in arteriole, capillary and venule

A

Arteriole = constriction, mast cell degranulation (chemotaxis, permeability, contraction endothelial) = fluid leakage
Capillary = platelet aggregation, emigration neutro, diapedesis or erythrocytes
Venules = emigration of lympho, infiltration of macro, fibrin deposition

44
Q

Composition of eosinophilic granules

A
  1. Small granules (acid phosphatase, arylsulfatase) = inactive leukotriene
  2. Primary granule
  3. Large specific granule :
    Major basic prot + Cationic prot = toxic parasites, histamine release
    Eosinophil-derived neurotoxin = microbicidal
    Eosinophil peroxidase = microbicidal
    Catalase = inactive leukotriene
45
Q

Enzymes and molecules in neutrophils

A

Specific granules :
- lactoferrin
- lysozyme
- alkaline phosphatase
- collagene 4
- leuco adhesion molecule, plasminogen activation, phospholipase A2
Azurophilic granules :
- MPO
- lysozyme
- cationic prots
- acid hydrolase
- elastase
- Non-sp collagenase
- BPI
- defensin, cathepsin
- phospholipase A2

46
Q

To which cytokines respond neutrophils and monocytes

A

Neutro = IL8
Monocytes = CX3CL1, CXCL1, CCL2

47
Q

Receptors of PAMPs
1. TLR6, TLR2, TLR1
2. TLR4-CD14, MD-2
3. TLR7-TLR8
4. TLR3
5. TLR5
6. TLR9
7. TLR10-11

A
  1. TLR6, TLR2, TLR1
    - peptidoglycans G+
    - lipoprotein
    - mycobacterie
    - LPS (lepto)
    - GPI (trypanosoma)
    - Zymosan (yeast)
  2. TLR4-CD14, MD-2
    - LPS G-
    - Lipoteichoic acids G+
    - RSV F protein
  3. TLR7-TLR8
    - ssRNA
  4. TLR3
    - dsRNA
  5. TLR5
    - Flagellin
  6. TLR9
    - Unmethylated CpG DNA
  7. TLR10-11
    - Uropathogenic bacteria
48
Q

Activity of :
1. a defensin
2. B defensin
3. Cathelicidins
4. Surfactant prots A et D

A
  1. a defensin (entero, leuco)
    microbidice, induce IL8, inhibe angiogenesis
  2. B defensin (epithelia, leuco)
    microbidice, chemotaxis (neutro, DC, leuco = prolif)
  3. Cathelicidins (leuco, epithelia)
    microbicide, cytokine/histamine release, cell prolif, angiogenesis, wound healing, prevent apopto (PR39)
  4. Surfactant prots A et D (epithelia)
    opsonize, macro activation
49
Q

Th2 response

A

IL2-4-5-10-13-17-19
CCL3, 4, 5, 11

50
Q

Th1 response

A

IL2-12-17-23, IFNy, TNF
CCL3,4,5 CCL2,3,4,5,7,8,12, CXCL9

51
Q

What is the response with tissue macrophage activated by IFNy?

A

Inflammation and tissue injury = ROS, protease, cytokine, chemokines, coag factor, AA metabolites

52
Q

What is the response with tissue macrophage activated by IL4?

A

Repair = growth factor (PDGF, FGF, TGFB), fibrogenic cytokines, angiogenic factor, remodeling collagenesis

53
Q

How are classically activated macrophages induced?

A

By microbial products and cytokines (IFNy)

54
Q

How are alternatively activated macrophages induced?

A

Cytokines (IL4, IL13) and in response to helminths

55
Q

classically activated macrophage response

A

ROS, NO, lysosomal enzyme = microbidice
IL1, IL12, IL23, chemokines = inflamm

56
Q

alternatively activated macrophages response

A

IL10 TGFB = antiinflamm
Arginase, proline, polyaminase, TGFB = wound repair, fibrosis

57
Q

HIF-a in hypoxic or normal conditions

A

Normal :
HIF-a hydroxylation prevents binding to P300BP
Hypoxic :
HIF-a not hydroxylated = binds P300BP = gene transcription of the HRE (hypoxia response element) = angiogenesis, iron sequestration, hypoxia metabolism

58
Q

Mechanism of TGF-B for collagene proliferation

A

TGF-B -> R-SMAD phospho = transcription for ECM depot, myofibroblast differenciation and fibroblast activation
regulated by SMAD 7

59
Q

What does Th1 produce?

A

IFNy = active macro classical pathway

59
Q

What does Th2 produce?

A

IL4, IL5, IL13 = recruit eosino, macro M2

60
Q

What does Th17 produce?

A

IL 17 and other = secretion of chemokines, recruitment of neutrophils and monocytes

61
Q

Formation of granuloma

A

M1 activated -> IL12 + present AG to CD4+ Th1 LT = epithelioid cell, giant cell, fibroblast, lympho, M1
FOREIGN BODY GRANULOMA = absence of LT immune response
IMMUNE GRANULOMA = peristent LT response (Th1 produce IFNy)

62
Q

Proliferation of hepatocytes in response to injury

A

1- priming phase = IL6 produced by Kupffer act on hepatocytes to receive GF
2- GF phase = HGF, TGFa stimulate metabolism, DNA replication
3- termination phase = return to quiescence (TGFB)

63
Q

Steps of angiogenesis

A
  1. VasoD (NO, VEGF)
  2. separation of pericytes (break basement membrane)
  3. migration of endothelial cell -> proliferation
  4. remodeling of capillary tubules
  5. recruitment of periendothelial cells (pericytes)
  6. suppression of endothelial proliferation
64
Q

Notch pathway in angiogenesis

A

regulates sprouting and branching (stimulated by VEGF)

65
Q

PDGF and TGFB in angiogenesis

A

STABILISATION
PGDF = recruit smooth muscle cell
TGFB = suppress endothelial prolif/migration

66
Q

When can it heal by first intention?

A

When it involves only the epithelial layer

67
Q
A

Nutrition (13 decks)

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