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Inflammation and Cytokines > Inflammation and Cytokines > Flashcards

Inflammation and Cytokines Flashcards

1
Q

Injury

A
  • leads to exposed collagen, platelet activating factor release, tissue factor release from endothelium
  • platelets bind - release important growth factors (PDGF); leads to PMN, macrophage recruitment
  • macrophages play dominant role in wound healing, release important growth factors (PDGF) and cytokines (IL-1 and TNF-alpha)
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2
Q

PDGF

A
  • similar effect as TGF-B
  • 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
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3
Q

EGF (epidermal growth factor)

A
  • acts on similar receptors as TGF-B; less potent
  • chemotactic and activates fibroblasts –> collagen and ECM proteins
  • angiogenesis –> VEGF stimulates angiogenesis and is involved in tumor mets
  • epithelialization
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4
Q

Fibroblastic growth factor (FGF)

A
  • chemotactic and activates fibroblasts –> collagen and ECM proteins
  • angiogenesis
  • epithelialization
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5
Q

PAF (platelet activating factor)

A
  • not stored, generated by phospholipase in endothelium and other cells
  • stimulates many types of inflammatory cells; chemotactic; increase adhesion molecules
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6
Q

Chemotactic factors

A
  • for inflammatory cells: TGF-B, PDGF, IL-8, LTB-4, C5a and C3a, PAF
  • for fibroblasts: TGF-B, PDGF, EGF, FGF
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7
Q

Angiogenesis Factors

A

TGF-B, EGF, FGF, TGF-alpha, IL-8, hypoxia

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8
Q

Epithelialization factors

A

TGF-B, PDGF, EGF, FGF, TGF-aplha

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9
Q

PMNs

A

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

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10
Q

Platelets

A

last 7-10 days

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11
Q

Lymphocytes

A

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

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12
Q

Eosinophils

A
  • involved in type I hypersensitivity rxn
  • have IgE receptors that bind to allergen
  • release major basic protein, which stimulates basophils and mast cells to release histmaine
  • increased in parasitic infections
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13
Q

Basophils

A
  • involved in type I hypersensitivity rxn
  • have IgE receptors
  • main source of histamine in blood; not found in tissue
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14
Q

Mast cells

A
  • primary cell in type I hypersensitivity rxn

* main source of histamine in tissues other than stomach

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15
Q

Histamine

A
  • vasodilation, tissue edema, postcapillary leakage

* primary effectors in type I hypersensitivity rxs (allergic reactions)

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16
Q

Bradykinin

A
  • vasodilation, increased permeability, pain, contraction of pulmonary arterioles
  • Angiotensin converting enzyme (ACE) - inactivates bradykinin
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17
Q

Nitric oxide

A
  • has arginine precursor
  • activates guanylate cyclase and increases cGMP, resulting in vascular smooth muscle dilation
  • is also called endothelium-derived relaxing factor
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18
Q

Endothelin

A

vascular smooth muscle contraction

19
Q

Initial cytokine response to injury and infection

A

TNF-alpha and IL-1

20
Q

Tumor necrosis factor alpha (TNF-alpha

A
  • macrophages - largest producers of TNF
  • increases adhesion molecules
  • overall a procoagulant
  • causes cachexia in patients with cancer
  • activates neutrophils and macrophages –> more cytokine production, cell recruitment; can also cause myocardial depression
  • fever, hypothermia, tachycardia, increase cardiac output, decrease SVRI –> high concentrations can cause circulatory collapse and multisystem organ failure
21
Q

IL-1

A
  • main source also macrophages; effects similar to TNF and synergizes TNF
  • responsible for fever (PGE2 mediated in hypothalamus) –> raises thermal set point, causing fever; NSAIDs decrease fever, reducing PGE2 synthesis
  • alveolar macrophages –> cause fever with atelectasis by releasing IL-1
  • IL-1 also increases IL-6 production
22
Q

IL-6

A
  • increase hepatic acute phase proteins (CRP, amyloid A)

* lymphocyte activation

23
Q

Interferons

A
  • released by lymphocytes in response to viral infection or other stimulates
  • activate macrophages, NK cells, and cytotoxic T cells
  • inhibit viral replication
24
Q

Hepatic Acute Phase Response Proteins

A
  • IL-6 most potent stimulus
  • increased: CRP (an opsonin, activates complement), amyloid A and P, fibrinogen, haptoglobin, ceruloplasmin, alpha-1 antitrypsin, alpha-1 antichymotrypsin and C3 (complement)
  • decreased: albumin and transferrin
25
Q

Selectins

A

*L-selectins, located on leukocytes, bind to E-(endothelial) and P-(platelets) selectins; rolling adhesion

26
Q

Beta-2 integrins

A

CD 11/18 molecules - on leukocytes; bind ICAMs, anchoring adhesion

27
Q

ICAM, VCAM, PECAM, ELAM

A

*on endothelial cells, bind beta-2 integrin molecules located on leukocytes and platelets; these are also involved in transendothelial migration

28
Q

Classic pathway

A
  • IgG or IgM - antigen-antibody complex activates
  • factors C1, C2 and C4 - found only in classic pathway
  • C3 - common to and is the convergence point for both pathways
  • Mg required for both pathways
  • Membrane attack complex - C5b-C9b
29
Q

Alternative pathway

A
  • endotoxin, bacteria, other stimuli activate
  • factors B, D, and P (properdin) - found only in alternate pathway
  • C3 - common to and is the convergence point for both pathways
  • Mg required for both pathways
30
Q

C3b

A

opsonization

31
Q

C3a and C5a

A

chemotaxis

32
Q

PGI2 and PGE2

A

vasodilation, bronchodilation, increase permeability, inhibit platelets

33
Q

PGD2

A

vasodilation, bronchoconstriction, increase permeability

34
Q

NSAIDs

A

inhibit cyclooxygenase (reversible)

35
Q

Aspirin

A

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

36
Q

Steroids

A

inhibit phospholipase, which converts phospholipids to arachidonic acid –> inhibits inflammation

37
Q

Leukotrienes: LTC4, LTD4, LTE4

A

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

38
Q

LTB4

A

chemotactic

39
Q

Cathecholamines

A
  • peak 24-48 hours after injury
  • norepinephrine released from sympathetic postganglionic neurons
  • epinephrine and norepinephrine released from adrenal medulla (neural response to injury)
40
Q

Neuroendocrine response to injury

A

afferent nerves from site of injury stimulate CRF, ACTH, ADH, growth hormone, epinephrine and NE release
*thyroid hormone does NOT play a major role in injury

41
Q

CXC chemokines

A
  • chemotaxis, angiogenesis, wound healing
  • IL-8 and platelet factor 4 are CXC chemokines
  • C = cysteine X –> another amino acid
42
Q

Red blood cells

A

*have some antioxidant properties (superoxide dismutase and catalase)

43
Q

Reperfusion injury

A

PMNs are primary mediator

44
Q

Chronic granulomatous disease

A

NADPH-oxidase system enzyme defect in PMNs; results in decrease superoxide radical (O2-) formation

Inflammation and Cytokines (1 decks)

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