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Pathology > Unit II: Inflammatory Mediators > Flashcards

Unit II: Inflammatory Mediators Flashcards

1
Q

IL-7

  • downstream signaling
  • associated disease?
A
  • JAK/STAT
  • IL-7 gamma receptor unit defect= SCID
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2
Q

Why is inflammation difficult to treat?

A

Functional redundancy–

  • mediators have multiple functions and functions can have multiple mediators,
  • inflammation can be triggered by multple forms of injury
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3
Q

Growth factor receptors

A

RTKs

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4
Q

NF-kß

  1. activation (upstream)
  2. inhibition
  3. function
A
  1. TNF receptors
  2. corticosteroids
  3. IL-1,6, TNF
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5
Q

Plasma proteins

  1. function
  2. time
  3. area
  4. types (x5)
  5. Mechanisms of activation? (x3)
A
  1. inactive components (serine proteases). Amplify inflammatory response
  2. mins–> hours
  3. local activation
    • coagulation proteins= Haegman factor, plasmin
    • firbinopeptides (fibrin degradation products)
    • complement proteins (C3a, C5a, C3b)
    • kinins
    • immunoglobulins
  5. injury associations
    • negatively charged surfaces (BM, collagen)
    • LPS
    • Enzymes (trypsin, plasmin)
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6
Q

Lipid mediators- what are they? timeline? purpose?

A
  • must be synthesized. Examples:
    • platelet activating factor,
    • arachidonic acid products (PGs, LTs, TX, PGI, SRS-As)-
  • mins= early migration of leukocytes
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7
Q

Protein Mediators

A
  • Ex: cytokines (monokines, lymphokines) ILs, GFs
  • mediate later phase of inflammation (must be synthesized)
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8
Q

Platelet activation

A

from trauma=> release of serotonin, thromboxane

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9
Q

Activation of “sentry” macrophages

A

from exotoxins, LPS, superantigens==> IL-1 production

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10
Q

Vasoactive amines

A

histamine (from mast cells)

Serotonin (from platelets)

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11
Q

What histamine receptor mediates inflammation?

Histamine release from mast cells can be due to (x6)

A

H1 receptor= inflammation

  1. trauma/cold
  2. IgE
  3. C3a, C5a
  4. histamine releasing factors from neutros, monocyts, platelets
  5. IL-1
  6. Toll receptor activation by LPS and peptidoglycan of G+ bacteria
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12
Q

Serotonin release from? receptor it acts on?

A
  • activated platelets; 90% of serotonin found in enterochromaffin cells in GI tract.
  • acts through 5HT receptors
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13
Q

Inflammatory responses to

  1. Histamine
  2. Serotonin
  3. Both
A
  1. axonal reflex of flare response
  2. aggregation of platelets
  3. SM contraction, vasodilation, increased vascular permeability, pain stimulator, itching
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14
Q

Fibrinolysis- how, function?

A

Fibrin cleaved by plasmin

function: fibrin degradation producints increased vascular permeability in skin and lungs

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15
Q

4 things Haefeman factor activates

A

Hageman factor= Factor 12a

  • plasminogen==> plasmin= fibronolysis
  • complement activation- C3a, C5a= anaphylotoxins
  • clotting cascade
  • activation of kallikrein==> kinin
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16
Q

Anaphylotoxin (x2) mechanisms

      1. one does some extra stuff
A

C3a and C5a.

  1. increased vascular permeability
  2. smooth muscle contrction
  3. C5a= neutrophil chemotaxis, degranulation, superoxide production
17
Q

Phosphatidylcholine==> ______

enzyme?

A
  • phosphatidyl choline==> arachidonic acid
    • Phospholipase A2
18
Q

Phosphatidylserine==>

A

phosphatidylserine==> DAG ==> arachidonic acid

  • Enzymes: Phospholipase C ; diacylglycerol lipase
19
Q

bradykinin inactivation

A

ACE

ACEi = increased bradykinin levels==> nuisance cough

20
Q

Prostaglandins

  1. what cell are they made in? what enzyme is used?
  2. PGD2/E2- functions
  3. PGF2a- functions
A
  1. cyclooxygenase, made in macrophages
  2. PGD2/E2= vasodilation, increased vascular permeability, pain, bronchoconstriction
  3. bronchoconstriction, vasodilation
21
Q

Prostacyclin (PGI2)

  1. where is it made, what enzyme
  2. functions
A
  1. endothelial cells, cyclooxygenase
  2. vasodilation, increased vascular permeability, inhibits PMNs, inhibits platelet aggregation
22
Q

Thromboxane

  1. where is it made, enzyme
  2. functions
A
  1. platelets, cyclooxygenase
  2. vasoconstriction, bronchoconstriction, platelet aggregation, antagonizes prostacyclin
23
Q

SRSA’s-

  1. where are they made, enzyme
  2. functions
  3. blocked by?
A

LTC4,D4, E4

  1. lipooxygenase, mast cells
  2. anaphylaxis: contraction of smooth muscle (vasoconstriction, bronchoconstriction), increased vascular permeability
  3. lipotoxins block SRS-A receptors
24
Q

LTB4

  1. where is it formed, enzyme
  2. function
A
  1. lipoxygenase, neutrophils (mainly, but also in endothelial cells)
  2. mediate neutrophil response via: chemotaxis, aggregation, degranulation
25
Q

PAFs

  1. where are they made, enzyme used
  2. functions (x5)
A
  1. acetylated lysophospholipid- mast cells, basophils, neutrophils, macrophages
    • platelet aggregation and degranulation,
    • release of histamine and serotonin,
    • increased vascular permeability,
    • increased leukocyte adhesion,
    • chemotoxis
26
Q

Lipotoxins

  1. where are they made, from what? structure is similar to?
  2. functions
A
  1. neutrophils, monocytes and macrophages, from arachidonic acid–similar to LT
  2. anti-inflammatory, block SRS-A receptor, increased leukocyte adhesion, chemotaxis
27
Q

Early LIPID mediators- action and mediator

  1. 2.
A

Early lipid mediators= platelets and mast cells

  1. platelet aggregation= TXA2 (platelets), PAF (mast cells)
  2. Increased vascular permeability= SRS-A (mast cells and platelets)
28
Q

Middle platelet mediators

A

Middle platelet mediators= neutrophils, mast cells

  1. Chemotaxis= LTB4 (Neutro), PAF (mast cells), SRS-A (mast cells)
  2. Sustaining Vasc Perm- SRS-A; LTB4
29
Q

Late lipid mediators

A

neutrophils, macrophages

  1. vascular permeability, vasodilation- SRS-A (neutros); PGs (MQs)
30
Q

Lymphokines- define, give example

A

cytokines that control lymphocyte response

ex: IL-1 (from macrophages)==> increaed IL-2 Receptors on T-cells==> increased IL-2 GF

31
Q

IL-1, 6, TNF-a

  1. Systemic response- what are they, which ones?
  2. local effects (x3)
  3. 4.
A
  1. Systemic (IL-1) Fever, acute phase response, leukocytosis
  2. Endothelial cells: leukocyte adhesion, cytokine synthesis
  3. Fibrobralst: proliferation, collagen synthsis
  4. Leukocytes: increased cytokine secretion
32
Q

Chemokines

  1. receptors
  2. structures
  3. co-receptors for HIV?
A
  1. GPCR;
  2. C-C= chemokine with adjacent cysteines; CXC= amino acid separates two cysteines
  3. CSCR4, CCR5= coreceptors for HIV
33
Q

IFN-Gamma

  1. released from
  2. acts on
  3. function
A

Augment cellular immune response and inflammation (ex: granuloma)

  1. t-cells, NK cells
  2. leukocytes, tissue cells, TH2 cells
  3. induce MHC I/II expression, activates phagocytosis, inhibits TH2, enhances leukocyte endothelial adherence
34
Q

TGF-Beta- function

A

fibrogenesis, scar healing

35
Q

IL-12

A
  • made by lymphocytes
  • Fxn: Lymphocyte proliferation, IL-2 production, IL-2 receptors
36
Q

Chemokines for:

  1. neutrophils
  2. monocytes
  3. eosinophils
A
  1. IL-8/CXC8= neutrophil adhesion and migration
  2. MCP= monocyte migration
  3. RANTES/MCP3= eosinophil migration
37
Q

NO

  1. synthesis
  2. expression
  3. endhances
  4. inhibits
A
  1. Arginine==> NO; NO synthase
  2. eNOS, nNOS (endothelial, neuron) always expressed. iNOS= induced in inflammation
  3. vasodilation, platelet aggregation, bacteriocidal
  4. inhibits leukocyte migration
38
Q
A
39
Q
A

Pathology (7 decks)

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