Chapter 13: Inflammation and Cytokines Flashcards Preview

ABSITE. > Chapter 13: Inflammation and Cytokines > Flashcards

Flashcards in Chapter 13: Inflammation and Cytokines Deck (70):
1

Leads to exposed collagen, platelet-activating factor release and tissue factor release from endothelium

Injury

2

What happens when platelets bind collagen?

Release growth factors (platelet-derived growth factor [PDGF]); leads to PMN and macrophage recruitment

3

Dominant role in wound healing; release important growth factors (PDGF) and cytokines (IL-1 and TNF-alpha)

Macrophages

4

- Chemotactic and activates inflammatory cells (PMNs and macrophages)
- Chemotactic and activates fibroblasts -> collagen and ECM proteins
- Angiogenesis, epithelialization, chemotactic for smooth muscle cells, has been shown to accelerate wound healing

PDGF

5

- Chemotactic and activates fibroblasts
- Angiogenesis
- Epithelialization

EGF (epidermal growth factor)

6

- Chemotactic and activates fibroblasts -> collagen and ECM proteins
- Angiogenesis
- Epithelialization

FGF (fibroblastic growth factor)

7

- Is not stored, generated by phospholipase in endothelium; is a phospholipid
- Chemotactic for inflammatory cells; increase adhesion molecules

PAF (platelet-activating factor)

8

Chemotactic factors: for inflammatory cells

PDGF, IL-8, LTB-4, C5a and C3a, PAF

9

Chemotactic factors: for fibroblasts

PDGF, EGF, FGF

10

Angiogenesis factors

PDGF, EGF, FGF, IL-8, hypoxia

11

Epithelialization factors

PDGF, EGE, FGF

12

Last 1-2 days in tissues (7 days in blood)

PMNs

13

Lasts 7-10 days

Platelets

14

Involved in chronic inflammation (T cells) and antibody production (B cells)

Lymphocytes

15

Growth and activating factors

PDGF, EGF, FGF, PAF, (Chemotactic, angiogenesis, epithelialization), PMNs, platelets, lymphocytes, TXA2, PGI2

16

- Have IgE receptors that bind to allergen
- Release major basic protein, which stimulates basophils and mast cells to release histamine
- Increased in parasitic infections

Eosinophils

17

What do eosinophils release?

Major basic protein, which stimulates basophils and mast cells to release histamine

18

Main source of histamine in blood; not found in tissue

Basophils

19

- Primary cell in type 1 hypersensitivity reactions
- Main source of histamine in tissues

Mast cells

20

- Vasodilation, tissue edema, postcapillary leakage
- Primary effector in type 1 hypersensitivity reactions (allergic reactions)

Histamine

21

Peripheral vasodilation, increased permeability, pain, pulmonary vasoconstriction

Bradykinin

22

Inactivates bradykinin; located in lung

Angiotensin-converting enzyme (ACE)

23

Cells involved in type 1 hypersensitivity reactions

Eosinophils, basophils, mast cells, histamine, bradykinin

24

Substrate for nitric oxide synthase

Arginine

25

Activates gauntlet cyclase and increases cGMP, resulting in vascular smooth muscle dilation
- AKA: endothelium-derived relaxing factor

Nitric Oxide (NO)

26

Causes vascular smooth muscle constriction (opposite effect of nitric oxide)

Endothelin

27

Main initial cytokine response to injury and infection

TNF-alpha and IL-1

28

Largest producers of TNF

Macrophages

29

- Increases adhesion molecules
- Overall, a procoagulant.
- Causes cachexia in patients with cancer.
- Activates neutrophils and macrophages

TNF-alpha

30

What can high concentrations of TNF-alpha cause?

Circulatory collapse and multisystem organ failure

31

- Main source macrophages; effects similar to TNF-alpha and synergizes TNF-alpha
- Responsible for fever (PGE2 mediated in hypothalamus)

IL-1

32

Cause fever with atelectasis by releasing IL-1

Alveolar macrophages

33

Increases hepatic acute phase proteins (C-reactive protein, amyloid A)

IL-6

34

- Released by lymphocytes in response to viral infection or other stimulants
- Active macrophages, natural killer cells, and cytotoxic T cells
- Inhibit viral replication

Interferon

35

Most potent stimulus for hepatic acute phase response proteins

IL-6

36

Hepatic acute phase response proteins
- Increased?
- Decreased?

- Increased: CRP, amyloid A and P, fibrinogen, haptoglobin, ceruloplasmin, alpha-1 antitrypsin, and C3 (complement
- Decreased: albumin, pre-albumin, and transferrin

37

An opsonin, activates complement

C-reactive protein

38

- On leukocytes
- Bind ICAMs, etc
- Anchoring adhesion

Beta-2 integrins (CD 11/18 molecules)

39

- On endothelial cells, bind beta-2 integrin molecules located on leukocytes and platelets
- Also involved in transendothelial migration

ICAM, VCAM, PECAM, ELAM

40

What activates the classic complement pathway (IgG, or IgM)?

Antigen-antibody complex activates

41

Factors found only in the classic pathway

Factors C1, C2, and C4

42

What activates the alternative complement pathway?

Endotoxin, bacteria, other stimuli activate

43

Factors found only in the alternative pathway

Factors B, D, and P (properdin)

44

Complement: common to and is the convergence point for both pathway (alternative and classic)

C3

45

Complement: required for both pathways

Magnesium

46

- Increase vascular permeability, bronchoconstriction
- Activate mast cells and basophils

Anaphylatoxins (C3a, C4a, C5a)

47

What is the membrane attack complex?

C5b-9b, causes cell lysis (usually bacteria) by creating a hole in the cell membrane

48

Complement: opsonization (targets antigen for immune response)

C3b and C4b

49

Complement: chemotaxis for inflammatory cells

C3a and C5a

50

Produced from arachidonic precursors

Prostaglandins, Leukotrienes

51

Prostaglandins:
- Vasodilation
- Bronchodilation
- Increased permeability
- Inhibits platelets

PGI-2 and PGE-2

52

Inhibits cyclooxygenase (reversible)

NSAIDs

53

Inhibits cyclooxygenase (irreversible), inhibits platelet adhesion by decreasing TXA2

Aspirin

54

Inhibits phospholipase, which converts phospholipids to arachidonic acid -> inhibits inflammation

Steroids

55

Leukotrienes: slow-reacting substances of anaphylaxis; bronchoconstriction, vasoconstriction followed by increased permeability (wheal and flare)

LTC-4, LTD-4, LTE-4

56

Leukotrienes: chemotactic for inflammatory cells

LTB-4

57

Peaks 24-48 hours after injury

Catecholamines

58

Released from sympathetic postganglionic neurons

Norepinephrine

59

Released from the adrenal medulla (neural response to injury)

Epinephrine and norepinephrine

60

Neuroendocrine response to injury

Afferent nerves from site of injury stimulate CRF, ACTH, ADH, GH, epinephrine, and norepinephrine release

61

Does not play a major role in injury or inflammation

Thyroid hormone

62

Function: CXC chemokines

Chemotaxis, angiogenesis, wound healing

63

What are IL-8 and platelet factor 4?

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

64

Generated in inflammation

Oxidants

65

Main producer: superoxide anion radical (O2-)

NADPH oxidase

66

Main producer: Hydrogen peroxidase (H2O2)

Xanthine Oxidase

67

Cellular defense: superoxide anion radical

Superoxide dismutase

68

Cellular defense: hydrogen peroxidase

Glutathione peroxidase, catalase

69

Primary mediator of reperfusion injury

PMNs

70

NADPH-oxidase system enzyme defect in PMNs
- Results in decreased superoxide radical (O2-) formation

Chronic Granulomatous Disease