Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Nutrition > Inflamm > Flashcards

Inflamm Flashcards

(68 cards)

Start Studying
1
Q

What are the 4 cardinals signs of inflammation?

A

redness
swelling
heat
pain
+/- loss of fct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is contraction of endothelial cells elicited?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

The cytoskeletal reorganisation permitting transcellular leakage is mediated by :

A

IL1, IL6, TNFa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where are P-selectin stored?

A

Exists preformed in Weibel-Palade body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

The expression of selectin is mediated by

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Molecules involved in migration

A

CD31, PECAM1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do leucocytes pierce basement membrane?

A

By secreting collagenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are exogenous chemoattractants?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are endogenous chemoattractants?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Steps of phagocytosis

A
  1. recognition
  2. engulfment
  3. killing and degradation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Neutrophils granules

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Macrophages content

A

acid hydrolase
collagenase
elastase
phospholipase
plasminogen activator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Action of a1-antitrypsin on neutrophils

A

major inhibitor of neutrophils elastase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

NET formation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is frustrated phagocytosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
How do LT contribute to acute inflammation?
produce IL17 inducinf secretion of chemokines to recruit leucocytes
26
What are the termination mechanisms of acute inflammation?
Termination begins by switching the type of AA metabolite to antiinflammatory lipoxins = liberation of antiinflamm cytokines TGFB and IL10
27
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
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
28
When is histamin released?
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
Where is serotonin present?
platelets and neuroendocrine cells (GI)
30
AA derived mediators (eicosanoids) binds to what?
GPCR
31
Action of AA metabolites : 1. PGI2, PGE1, PGE2, PGD2 2. TxA2, LTC4, D4, E4 3. LT C4, D4, E4 4. LT B4, HETE
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
Why is COX-2 selectif inhibitor and interesting option?
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
Source and actions of cytokines in acute inflammation : 1. TNF 2. IL1 3. IL6 4. Chemokines 5. IL17
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
Source and actions of cytokines in chronic inflammation : 1. IL12 2. IFNy 3. IL17
1. IL12 DC, macro increase production of IFNy 2. IFNy LT, NK cells active macro 3. IL17 LT recruits neutro and monocytes
35
Role and production of tumor necrosis factor (TNF)
Production of TNF signals by TLR and IL1 Roles : - endo activation (adhesion, mediators) - activation of leucocytes, IL1 - supress appetit (cachexia)
36
Role of C-X-C chemokines
act on neutro, IL8 secreted by macro, endo cells inducers = microbial products, IL1, TNF
37
C-C chemokines (MCP-1, CCL2, CCL11, MIP-1, CCL3) role
attract monocytes, eosino, baso, lympho
38
C chemokines (lymphotactin, XCL1) role
relatively Sp for lympho
39
CX3C chemokines (CX3CL1) role
1 - cell surface bound on endo cells = promot adhesion of monocytes and LT 2- soluble form = potent chemoattractant
40
By what are triggered the 3 pathways of the complement system?
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
Role of DAF, factor H and CD59
DAF = prevent formation of C3 convertase CD59 = inhibit formation of MAC Factor H = promote cleavage and destruction of C3b = inhibits alternative pathway
42
Mediators of : 1. VasoD 2. Permeability 3. Chemotaxis/recruitment/activation 4. Fever 5. Pain 6. Tissue damage
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
Events in arteriole, capillary and venule
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
Composition of eosinophilic granules
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
Enzymes and molecules in neutrophils
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
To which cytokines respond neutrophils and monocytes
Neutro = IL8 Monocytes = CX3CL1, CXCL1, CCL2
47
Receptors of PAMPs 1. TLR6, TLR2, TLR1 2. TLR4-CD14, MD-2 3. TLR7-TLR8 4. TLR3 5. TLR5 6. TLR9 7. TLR10-11
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
Activity of : 1. a defensin 2. B defensin 3. Cathelicidins 4. Surfactant prots A et D
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
Th2 response
IL2-4-5-10-13-17-19 CCL3, 4, 5, 11
50
Th1 response
IL2-12-17-23, IFNy, TNF CCL3,4,5 CCL2,3,4,5,7,8,12, CXCL9
51
What is the response with tissue macrophage activated by IFNy?
Inflammation and tissue injury = ROS, protease, cytokine, chemokines, coag factor, AA metabolites
52
What is the response with tissue macrophage activated by IL4?
Repair = growth factor (PDGF, FGF, TGFB), fibrogenic cytokines, angiogenic factor, remodeling collagenesis
53
How are classically activated macrophages induced?
By microbial products and cytokines (IFNy)
54
How are alternatively activated macrophages induced?
Cytokines (IL4, IL13) and in response to helminths
55
classically activated macrophage response
ROS, NO, lysosomal enzyme = microbidice IL1, IL12, IL23, chemokines = inflamm
56
alternatively activated macrophages response
IL10 TGFB = antiinflamm Arginase, proline, polyaminase, TGFB = wound repair, fibrosis
57
HIF-a in hypoxic or normal conditions
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
Mechanism of TGF-B for collagene proliferation
TGF-B -> R-SMAD phospho = transcription for ECM depot, myofibroblast differenciation and fibroblast activation regulated by SMAD 7
59
What does Th1 produce?
IFNy = active macro classical pathway
59
What does Th2 produce?
IL4, IL5, IL13 = recruit eosino, macro M2
60
What does Th17 produce?
IL 17 and other = secretion of chemokines, recruitment of neutrophils and monocytes
61
Formation of granuloma
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
Proliferation of hepatocytes in response to injury
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
Steps of angiogenesis
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
Notch pathway in angiogenesis
regulates sprouting and branching (stimulated by VEGF)
65
PDGF and TGFB in angiogenesis
STABILISATION PGDF = recruit smooth muscle cell TGFB = suppress endothelial prolif/migration
66
When can it heal by first intention?
When it involves only the epithelial layer
67

Nutrition (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions