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ABSITE > Fiber Chaper 13. INFLAMMATION AND CYTOKINES > Flashcards

Fiber Chaper 13. INFLAMMATION AND CYTOKINES Flashcards

1
Q

Three phases of inflammation

A
  1. Injury: causes exposed collagen, PAF and TF release
  2. Platelets bind collagen: release growth factors (platelet derived growth factor PDGF) and leads to PMN and macrophage recruitment
  3. Macrophages: dominant role in wound healing; release important growth factors (PDGF) and cytokines (IL-1 and TNF-a)
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2
Q

PDGF

A
  • chemotactic and activated inflammatory cells (PMHs and macrophages) and fibroblasts, which leads to collagen and ECM proteins
  • angiogenesis
  • epithelialization
  • chemotactic for smooth muscle cells
  • has been shown to accelerate wound healing
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3
Q

EGF

A

epidermal growth factor

  • chemotactic and activates fibroblasts
  • angiogenesis
  • epithelialization
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4
Q

FGF

A

fibroblastic growth factor

  • chemotactic and activates fibroblasts, which leads to collagen and ECM proteins
  • angiogenesis
  • epithelialization
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5
Q

PAF

A

platelet activating factor

  • is not stored, generated by phospholipase in endothelium, is a phospholipid
  • chemotactic for inflammatory cells; increases adhesion molecules
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6
Q

Chemotactic factors

A

For inflammatory cells: PDGF, IL-8, LTB-4, C5a, C3a, PAF

For fibroblasts: PDGF, EGF, FGF

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7
Q

Angiogenesis factors

A

PDGF, EGF, FGF, IL-8, hypoxia

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8
Q

Epithelialization factors

A

PDGF, EGF, FGF

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9
Q

PMNs last how long?

A

1-2 days in tissues, 7 days in blood

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10
Q

Platelets last how long?

A

7-10 days

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11
Q

Lymphocytes do what?

A

Chronic inflammation (T cells) and antibody productions (B cells)

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12
Q

Type 1 Hypersensitivity (allergic reactions)

A
  • Eosinophils: IgE receptors that bind to allergen, release major basic protein, which stimulates basophils and mast cells to release histamine; increased in parasitic infections
  • Basophils: main source of histamine in blood; not found in tissue
  • Mast cells: primary cell in type 1 hypersensitivity reactions; main source of histamine in tissues
  • Histamine: vasodilation, tissue edema, postcapillary leakage; primary effector in type 1 hypersensitivity reactions
  • Bradykinin: peripheral vasodilation, increased permeability, pain, pulmonary vasoconstriction (inactivated by ACE)
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13
Q

What is the main source of histamine in blood? Tissues?

A

Blood: basophils

Tissue: mast cells

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14
Q

What does histamine do?

A
  • Released by basophils (in blood) and mast cells (in tissue) in response to major basic protein released by eosinophils (which have IgE receptos which bind allergen)
  • Vasodilation, tissue edema, postcapillary leakage
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15
Q

What causes peripheral vasodilation, increased permeability, pain, and pulmonary vasoconstriction in a type 1 hypersensitivity reaction?

A

Bradykinin

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16
Q

What inactivates bradykinin?

A

ACE; located in lung

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17
Q

Nitric oxide

A

also called endothelium derived relaxing factor

arginine -> (via NOS) -> nitric oxide

NO activates guanylate cyclase and increases cGMP resulting in vascular smooth muscle dilation

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18
Q

What is the precursor to nitric oxide?

A

arginine

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19
Q

What does NO do?

A

activated guanylate cyclase and increases cGMP to cause vascular smooth muscle dilation

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20
Q

What does the opposite of NO?

A

Endothelin (causes vascular smooth muscle constriction)

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21
Q

Main initial cytokine response to injury and infection

A

TNF-alpha and IL-1 release

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22
Q

TNF-alpha

A
  • Macrophages are largest producers of TNF-a
  • Increases adhesion molecules
  • Procoagulant
  • Cachexia in cancer patients
  • Activates neutrophils and macrophages -> more cytokine production and cell recruitment
  • High concentrations can cause circulatory collapse and multisystem organ failure
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23
Q

IL-1

A
  • Macrophages are main source
  • Effects similar to TNF-a and synergized TNF-a
  • Responsible for fever (PGE2 mediated in hypothalamus): raises thermal set point, NSAIDs can decrease fever by reducing PGE2 synthethis
  • Alveolar macrophages: cause fever with atelectasis by releasing IL-1
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24
Q

What cytokine causes fever?

A

IL-1

25
Q

What cytokine causes cachexia?

A

TNF-a

26
Q

IL-6

A

Increases hepatic acute phase proteins (CRP and amyloid A)

27
Q

What are interferons?

A

Released by lymphocytes in response to viral infection or other stimulants

  • Activate macrophages, natural killer cells, and cytotoxic T cells
  • Inhibit viral replication
28
Q

Hepatic acute phase response proteins

A
  • IL-6: most potent stimulus
  • CRP: opsonin, activates complement
  • Amyloid A and P
  • Fibrinogen
  • Haptoglobin
  • Ceruloplasmin
  • Alpha-1 antitrypsin
  • C3
  • (albumin, pre-albumin, and transferrin are DECREASED)
29
Q

Cell adhesion molecules

A

-Selectins, bet-2 integrins, ICAM, VCAM, PECAM, ELAM

30
Q

Selectins

A

L-selectins on leukocytes, bind to E- (endothelial) and P- (platelet) selectins all causing ROLLING ADHESIONS

31
Q

Beta-2 integrins

A

(CD 11/18 molecules) on leukocytes bind ICAMs, etc., ANCHORING ADHESION

32
Q

ICAM, VCAM, PECAM, ELAM

A

On endothelial cells, bind beta-2 integrin molecules located on leukocytes and platelets ; also involved in TRANSENDOTHELIAL MIGRATION

33
Q

Complement pathways

A

Classic (IgG or IgM): antigen-antibody complex activates; factors C1, C2, C4

Alternative: endotoxin, bacteria, other stimulus activates; Factors B, D, P (properdin)

34
Q

Convergence cytokine in complement pathways

A

C3

35
Q

Factors C1, C2, C4 are in what pathway?

A

Classic

36
Q

Factors B, D, P are in what pathway?

A

Alternative

37
Q

What molecule do both pathways need?

A

Mg

38
Q

Anaphylatoxins

A

C3a, C4a, C5a (C3a and C5a are also chemotaxis)

-increase vascular permeability, bronchoconstriction, activate mast cells and basophils (to release histamine)

39
Q

Membrane attack complex

A

C5b-C9b; causes cell lysis (usually bacteria) by creating a hole in cell membrane

40
Q

Obsonization

A

Targets Ag for immune response

C3b and C4b

41
Q

C3b and C4b do what?

A

Opsonizatoin

42
Q

Prostaglandins come from what?

A

Arachidonic precursors (by COX?)

43
Q

What do PGI2 and PGE2 do?

A

Vasodilation, bronchodilation, permeability, inhibit platelets

44
Q

Prostaglandin pathway

A

Phospholipids -> (phospholipase) -> Arachidonic acid -> (COX) -> PGG2 -> (peroxidase) -> PGH2 which either goes to PGI2, PGD2, PGE2, or (via thromboxane synthase) to TXA2

-Prostaglandins are vasodilatory and inhibit platelet adhesions, while TXAs are thrombotic and vasoconstrictors

45
Q

NSAIDs MoA

A

Inhibit COX reversibly

46
Q

Aspirin MoA

A

Inhibits COX irreversibly and inhibits platelet adhesion by decreasing TXA2

47
Q

Steroids MoA

A

Inhibits phospholipase, which converts phospholipids to arachidonic acid, therefore inhibits inflammation

48
Q

Leukotrienes

A

LTC2, LTD4, LTE4: slow reacting substances of anaphylaxis; bronchoconstriction, vasoconstriction followed by increased permeability (wheal and flare)

LTB4: chemotactic for inflammatory cells

-Produced from arachidonic precursors

49
Q

How long after injury do catecholamines peak?

A

24-48 hours

50
Q

Where is epi and norepi released?

A

Epi: adrenal medulla

Norepi: sympathetic postganglionic neurons and adrenal medulla

51
Q

Neuroendocrine response to injury

A

Afference nerves from site of injury stimulate CRF, ACTH, ADH, GH, Epi, and Norepi release

52
Q

Does thyroid hormone play a major role in injury and inflammation?

A

No

53
Q

CXC chemokines (C= cysteine, X= another amino acid)

A
  • Chemotaxis, angiogenesis, wound healing

- IL-8 and PF4 are CXC chemokines

54
Q

Oxidants generated in inflammation

A

Superoxide anion radical (O2-); main producer oxidase is NADPH oxidase

Hydrogen peroxide (H2O2); main producer oxidase is canthine oxidase

55
Q

Cellular defense against superoxide anion radial O2-?

A

Superoxide dismutase, which converts it to hydrogen peroxide H2O2

56
Q

Cellular defense against Hydrogen peroxide H2O2

A

Glutathione peroxidase, catalase

57
Q

What is the primary mediator in reperfusion injury?

A

PMNs

58
Q

What is chronic granulomatous disease?

A

NADPH oxidase system enzyme defect in PMNs, resulting in decreased superoxide O2- radical formation

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