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CMBM Exam 3 > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Acute phase protein (APP) defined as

A
  • Protein whose concentration increases (pos. APP) or decreases (neg. APP) by 25% or more during inflammatory processes or disorder
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2
Q

Acute phase proteins (APP) synthesized where

A
  • Most synthesized in the liver (except gamma globulins; from plasma cells)
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3
Q

APP regulated by

A
  • Inflammatory cytokines *IL-6, IL-1Beta, TNF-alpha - Most regulated primarily at transcriptional level, but some post-transcriptional and transnational changes as well
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4
Q

Clinical relevance of APP

A
  • Reflect the presence and intensity of an inflammatory process - Useful as a diagnostic aid, helping to differentiate inflammatory from non-inflammatory conditions
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5
Q

APP that rise the most after inflammatory stimulus

A
  • C-reactive protein - Serum amyloid A
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6
Q

Serum vs. Plasma

A
  • Plasma still has active clotting factors *Inactivating them leaves you with serum
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7
Q

Alpha 1 globulin

A
  • alpha1- Antitrypsin
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8
Q

Alpha 1/Alpha 2 globulins

A
  • Ceruloplasmin
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9
Q

Alpha 2 globulins

A
  • Haptoglobin - alpha 2-macroglobulin
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10
Q

Beta 1 globulin

A
  • Transferrin
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11
Q

Beta 2 globulin

A
  • Fibrinogen
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12
Q

Globulins increased during infection

A
  • alpha 1 - alpha 2
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13
Q

Alpha 1 antitrypsin deficiency

A
  • Emphysema (adults) - cirrhosis (juvenile)
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14
Q

C-reactive protein (CRP) elevated during

A
  • Chronic inflammatory conditions - Cancer
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15
Q

CRP regulation

A
  • At the transcriptional level: IL-6 induces, other cytokines act synergistically to increase response
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16
Q

CRP functions

A
  • part of innate immune response - Ca++ dependent binding of phosphocholine (PCh) *PCh present on cell membranes of bacterial and fungal pathogens - Binds nuclear components of apoptotic or necrotic cells - Ligand-bound CRP is bound by C1q and activates the classical complement pathway - CRP may also help recruit phagocytes by binding Fc receptors
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17
Q

Lower elevated levels of CRP are associated with

A
  • Increase cardiovascular risk
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18
Q

Serum amyloid A structure

A
  • Family of apolipoproteins, some acute phase reactants, some constitutive - Contains alpha helix w/ beta pleated sheets
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19
Q

SAA regulation

A
  • Levels increase within hours of stimulus - Magnitude of increase may be larger than CRP - Induced by synergistic action of cytokines *IL-1, IL-6
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20
Q

SAA function

A
  • Precursor of amyloid A protein, major component of secondary amyloid plaques - Associates w/ HDL, replacing apolipoprotein A-1 *This is going to induce reverse cholesterol transport - Reduces storage of cholesterol esters in macrophages (decrease foam cells)
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21
Q

Altered properties of acute phase HDL

A
  • Cleared from the circulation more rapidly - 5x increased binding to macrophages - Enhanced uptake of HDL by macrophages
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22
Q

Fibrinogen regulation

A
  • Made in hepatocytes - Moderate APP - induced by IL-6, glucocorticoids, oncostatin-M Abundant in plasma, elongated shape, greatest effect on ESR - Allows the platelet to coagulate
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23
Q

Fibrinogen and its cleavage products functions

A
  • Immunosuppression - Proliferation - Haemostasis - Blood vessel tone - Angiogenesis - Cell migration
24
Q

Erythrocyte Sedimentation Rate (ESR)

A
  • Blood + anti-coagulant placed in vertical tube and measure rate of fall - Measures the distance that a vertical column of anticoagulated blood has fallen in one hour - Most widely used marker of inflammation - Indirect measure of APP, especially fibrinogen - Increased aggregation of rbc causes them to fall faster - Increased by high immunoglobins - changes in rbc size, shape can affect ESR - Progressive increase w/ age
25
Q

Alpha 1- antitrypsin structure

A
  • Single- chain protein w/ 3 oligosaccharide side chains - Over 75 plymorphic forms
26
Q

Alpha 1- antitrypsin regulation

A
  • Most made in liver, ~1% in monocytes - Levels increase 3-4 fold in acute phase - Induced by IL-6
27
Q

Alpha 1- antitrypsin function

A
  • One of the compensatory molecules that will limit the damage that takes place during acute inflammatory events - Inhibits trypsin, elastase, other proteases by forming inactive complexes *blunts the effect of quite a few of the extracellular components that neutrophils release - Protects elastic fibers in lung alveoli from excessive digestion by neutrophil elastase
28
Q

Deficiency of AAP causes

A
  • Emphysema - Cirrhosis
29
Q

Alpha 2-macroglobulin structure and properties

A
  • Very large glycoprotein w/ 4 identical subunits - Comprises 8-10% total plasma protein
30
Q

Alpha 2-macroglobulin regulation

A
  • Synthesized by hepatocytes, monocytes, astrocytes - Relative levels increased in nephrotic syndrome, due mainly to large size
31
Q

Alpha 2-macroglobulin function

A
  • Panprotease inhibitor *limits the collateral damage that some of the inflammatory mediator cells are going to do; plays a direct role at the site of inflammation - Transports ~10% of zinc in plasma (albumin transports the rest) - Binds cytokine and growth factors, appears to target them to particular cell types
32
Q

Transferrin structure and properties

A
  • Beta globulin - Negative acute phase protein - Single-chain glycoprotein w/ 2 binding sites for Fe3+
33
Q

Transferrin function

A
  • Carries Fe in blood - Presence of unbound sites protects against infection by Fe-dependent pathogens - Level of saturation changes w/ Fe availability *TIBC (transferrin iron binding capacity) increases in Fe deficient states
34
Q

Ferritin

A
  • 24 subunits surround a core of 3-4000 Fe3+ - 2 subunit isoforms, L and H - Mostly in tissues, but small amount in blood=indicator of Fe reserves
35
Q

Haptoglobin

A
  • Alpha 2 globulin - Pos. APP - Antioxidant properties - Binds extra-corpuscular HB - Stimulates angiogenesis
36
Q

Albumin

A
  • Small but very abundant - Accounts for 50-60% of protein in plasma - Responsible for 80% osmotic pressure of blood - Represents 25% of total protein synthesized in liver - Neg. APP - Rate of synthesis depends on nutritional status - Transports numerous substances in blood
37
Q

Transthyretin (prealbumin)

A
  • Migrates slightly ahead of albumin during electrophoresis - Neg. APP - Transports Vit. A (retinol) and thyroxine (though most transported by thyroxine binding protein) - Inhibits IL-1 production by monocytes and endothelial cells
38
Q

Lukotrienes

A
  • Arachidonic acid metabolite
  • Product of lipoxygenase
  • 5 LO (neutrophils): 5-HETE
  • Precursor of leukotrienes (LTC4, LTD4, LTE4); vasoconstriction and bronchospasm
39
Q

Lipoxins

A
  • Arachidonic acid metabolite
  • Leukocytes + platelets
  • Inhibit neutrophil adhesion and chemotaxis
40
Q

Cyclooxygenase

A
  • Arachidonic acid metabolite
  • Generate prostaglandins

*product of mast cells, endothelial cells, and macrophages

41
Q

PGD2

A
  • Prostaglandin
  • Secreted by mast cells
  • Vasodilation and increases vascular permeability
  • Chemoattractant for neutrophils
42
Q

PGE2

A
  • Prostaglandin
  • Secreted by many cell types
  • Vasodilation and increases vascular permeability
43
Q

ThromboxaneA2

A
  • Prostaglandin
  • Secreted by platelets
  • Vasoconstriction and promotes platelet aggregation
44
Q

eNOS

A
  • Produced constitutively by endothelium
  • Down regulates or limits leukocyte adhesion by down regulating the cell surface molecules that would assoc. w/ endothelial cells
  • Short acting
45
Q

iNOS

A
  • Produced by macrophages
  • Complex w/ROS to generate reactive nitrogen species as well as all the other antimicrobial intermediates that macrophages produce
46
Q

Nitric oxide

A
  • Product of nitric oxide synthase (NOS) acting on L-arginine
  • 3 forms of NOS

*eNOS

*nNOS

*iNOS

  • Endogenous compensatory mechanism that reduces inflammatory responses

*primarily eNOS

  • NO production is enhances in response to microbial infection

*primarily iNOS

47
Q

TNF principal sources and role in inflammation

A
  • Sources

*Macrophages

*Mast cells

*T lymphocytes

  • Role: Stimulates expression of endothelial adhesion molecules and secretion of other cytokines; systemic effects
48
Q

IL-1 principal sources and role in inflammation

A
  • Sources:

*Macrophages

*Endothelial cells

*Some epithelial cells

  • Role: Similiar to TNF; greater role in fever
49
Q

IL-6 principal sources and role in inflammation

A
  • Sources:

*Macrophages

*Other cells

  • Systemic effects (acute-phase response)
50
Q

Chemokines principal sources and role in inflammation

A
  • Sources:

*Macrophages

*Endothelial cells

*T lymphocytes

*Mast cells

*Other cell types

  • Role: Recruitment of leukocytes to site of inflammation; migration of cells to normal tissues
51
Q

Cytokines in acute inflammation

A
  • TNF
  • IL-1
  • IL-6
  • Chemokines
52
Q

Cytokines in chronic inflammation

A
  • IL-12
  • IFN-y
  • IL-17
53
Q

IL-12 principal sources and role in inflammation

A
  • Sources:

*Dendritic cells

*macrophages

  • Role: Increased production of IFN-y
54
Q

IFN-y principal sources and role in inflammation

A
  • Sources:

*T lymphocytes

*NK cells

  • Role: Activation of macrophages (increased ability to kill microbes and tumor cells)
55
Q

IL-17 principal sources and role in inflammation

A
  • Sources:

*T lymphocytes

  • Role: Recruitment of neutrophils and monocytes
56
Q

Principal mediators of inflammation

A

CMBM Exam 3 (7 decks)

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