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Disease and Defense > Mediators of Inflammation > Flashcards

Mediators of Inflammation Flashcards

1
Q

where are mediators produced?

A

site of inflammation
or
by liver and activated at site of inflammation

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2
Q

when are mediators produced?

A

soon! - on released/activated they are quickly decayed, inactivated, eliminated, inhibited

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3
Q

how do mediators work?

A

most act by binding specific receptors, some (enzyme, ROS) have broad and non-specific effects

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4
Q

derivation?

vasoactive amines

A

cell

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5
Q

derivation?

compliments

A

plasma protein

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6
Q

derivation:

NO

A

cell

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7
Q

derivation

coagulative factors?

A

plasma

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8
Q

derivations

ROS?

A

Cell

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9
Q

derivation

cytokines?

A

cell

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10
Q

derivation

kinin?

A

plasma

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11
Q

derivation

lysosomal enzymes?

A

cell

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12
Q

derivation

neuropeptides?

A

cell

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13
Q

derivation

platelet activation factor?

A

cell

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14
Q

derivation

arachidonic acid metabolites?

A

cell

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15
Q

Histamine and seratonin are examples of?

A

vasoactive amines

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16
Q

Histamine and seratonin

response time?

A

stored in cells and ready for release, allowing for quick response

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17
Q

histamine causes?

A

arterial dilation and endothelial contraction

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18
Q

histamine comes from (3)

A

mast
basophils
platelets

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19
Q

what inactivates histamine

A

histaminase

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20
Q

what causes mast cells to release their histamine (6)

A 
physical
immune (binding IgE)
compliment (c3a, c5a)
histamine releasing protein (from leukocytes)
neuropeptides 
cytokines (IL1, IL8)
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21
Q

Serotonin causes?

A

vasoconstriction to aid in clotting

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22
Q

where is serotonin?

A

present in platelet granules

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23
Q

Where does arachidonic acid derived from?

A

derived from cell membrane phospholipids and is transformed into a number of compounds that mediate inflammation and hemostasis

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24
Q

Cell sources of AA? (4)

A

leukocytes
mast cells
endothelium
platelets

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25
Q

AA inactivation?

A

spontaneous decay

enzymes

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26
Q

AA metabolite formation

2 pathways

A
  1. cyclooxygenase –> prostaglandins and thromboxanes

2. lipoxygenase –> leukotrienes and lipoxins

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27
Q

Where do NSAIDS play a role in AA pathway?

A

block COX (thus shut down prostaglandins and thromboxanes)

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28
Q

Where do glucocorticoids play a role in AA pathway?

A

block phosphlipase A (thus shut down whole AA pathway)

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29
Q

Prostaglandins contribute to which symptoms of inflammation?

A

dolor

calor

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30
Q

what determine which prostaglandins / thromboxanes are made?

A

the presence of specific enzymes

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31
Q

endothelial cells have which enzymes in AA metabolism

A

prostacyclin synthase - which produces PGI2 - a vasodilator and inhibitor of platelet aggregation - but don’t make TXA2, which has opposite effect

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32
Q

AA –> leukotrienes - what do they do?

A

mediate specific functions of inflammation

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33
Q

what does LTB4 do?

A

chemotactic agent for neutrophils

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34
Q

what do LTC4 LTD4 and LTE4 do?

A

cause vascular permeability

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35
Q

Lipoxins - what are they?

A

AA metabolites that are generated as leukocytes enter tissues

they antagonize leukotrienes and are anti-inflammatory (inhibit neutorphil chemotaxis and endothelial adhesion)

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36
Q

what is platelet activating factor?

A

A cell derived mediator of inflammation

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37
Q

how is platelet activating factor produced?

A

similar to AA - phospholipase A2 cleaves lipids from cell membranes

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38
Q

what does platelet activating factor do?

A

name is misleading - does much

  • platelet aggregation
  • vasodilation
  • vascular permeability
  • bronchoconstriction
  • stimulus for other mediators
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39
Q

what are cytokines?

A

cell derived mediators - specifically polypeptides that function as mediators in both the innate and adaptive immune system

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40
Q

what are important acute inflammatory cytokines? (5)

A 
TNF1
IL1
Chemokines (CXC, CC)
IFN gamma
IL-12
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41
Q

TNF & IL-1
Who produces them
what stimulates production
what do they do

A

produced in a range of cells, but especially macrophages, mast cells, endothelial cells

production is stimulated by microbial products, immune complexes, and T cell mediators

cause endothelial activation (leukocyte binding and recruitment)

also induce systemic effects of inflammation - fever, acute phase protein synthesis, etc.

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42
Q

what are chemokines

A

cytokines - specifically small proteins separated into 2 groups (CXC, CC) based on structure

43
Q

what are chemokine primary function?

A

chemotaxis - but also activate leukocytes

44
Q

CXC is chemotactic for

A

neutrophils

45
Q

CC is chemotactic for

A

variety of cells (e.g. eotaxin for eosinophils)

46
Q

Which cytokines are imporant chronic inflammation cytokines

A

IFN-gamma - stimulates classical macrophage activation

IL-12 - stimulates the growth and function of T cells

47
Q

What are ROS?

A

cell derived mediators of inflammation

48
Q

who releases ROS?

A

activated neutrophils and macrophages

49
Q

what are ROS made from?

A

NADPH oxidase pathway which produces superoxide radical

50
Q

what does superoxide spontaneously change to?

A

hydrogen peroxide which can also be converted to hypochlorous radical via myeloperoxidase in neutrophils

51
Q

What do ROS do?

A

highly toxic oxidizers that not only damage microbes, but also host tissue (endogenous antioxidants (e.g. superoxide dismutase) mitigate effect on host

52
Q

NO what is it / what does it do?

A

Nitric oxide is a cell derived mediator

Like ROS is is a free radical that can be used to kill microbes

It is also a mediator of vasodilation, antagonizes platelet activation, and reduces leukocyte recruitment

53
Q

What makes NO ?

A

Nitric oxide synthase (NOS) from L arginine (3 isoforms)

54
Q

What is Type II NOS?

A

Inducible NOS: induced in macrophages and endothelial cells

55
Q

What induces Type II NOS?

A

IL-1
TNF
IFN-gamma
bacterial endotoxins

56
Q

What is Type II NOS responsible for?

A

NO in inflammation (can also be induced in other cell types)

57
Q

What is type III NOS?

A

Endothelial NOS: constitutively expressed in endothelial cells

58
Q

What are the azurophil granules of neutrophils and granules of monocytes?

A

they are either similar to lysosomes or are modified lysosomes

59
Q

What do the granules of monocytes and neutrophils contain?

A

enzymes that can kill microbes and digest ingested materials

60
Q

In addition to containing enzymes that kill microbes and digest ingested materials, what else are granules a significant source of?

A

substances that damage normal host tissue -

  • acid proteases active within phagolysosomes (low pH)
  • neutral proteases (e.g. collagenases) are active outside the cell (neutral pH)
61
Q

What helps to minimize the damage that lysosomal enzymes do to host tissue?

A

protease inhibitors - present in blood and body tissue

  • alpha 1 antitrypsin
  • alpha 2 macroglobulin
62
Q

where are acid protease (lysosomal enzyme) active?

A

phagolysosomes (low pH)

63
Q

where are neutral proteases (E.g. collagenase) active?

A

outside the cells (neutral pH)

64
Q

what does alpha 1 antitrypsin do

A

neutrophil elastase inhibitor

65
Q

what does alpha 2 macroglobulin do?

A

inhibits a large variety of proetinases (e.g. collagenase)

66
Q

are all granules in neutrophils the same?

A

no - they have different constituents and function differently which includes tendency for extra-versus intra-cellular activity

67
Q

what are nueropeptides and what do they do

A

cell derived mediator

can initiate inflammation

68
Q

when and where are neuropeptides active?

A

in vascular tone and permeability

particularly in lung and GI

69
Q

Substance P is what?

A

a neuroactive peptide (11 aa)

70
Q

who secretes substance P

A

nerves and inflammatory cells (macs, eos, lymphs, dends)

71
Q

what does substance P do?

A

binds to neurokinin-1 receptor to generate a pro-inflammatory effec in immune ant epithelial cells

72
Q

compliment - where is it from

A

plasma protein derived

73
Q

what does compliment do?

A

opsonize pathogens and induce a series of inflammatory responses that help to fight infection

specific immune functions include increasing vascular permeability and luekocyte chemotaxis

74
Q

what does the final activated compliment do?

A

forms membrane attack complex (MAC) that forms holes in the membranes of microbes

75
Q

under normal conditions what are the compliment dudes doing?

A

components of compliment system (C1-9) circulate as inactive molecules in the plasma

76
Q

what activates compliment

A

proteolysis

77
Q

what happens once compliment is activated

A

the components are able to proteolyze and amplify the reaction

78
Q

What is the key factor in compliment

A

c3 convertase that cleave c3 into c3a and c3b

79
Q

what does c3b do

A

binds to c3 convertase to from c5 convertase, which initates c5b-9 formation (The MAC)

80
Q

What are the three separate pathways that lead to C3 convertase formation

A
  1. classical
    2 alternative
  2. lectin
81
Q

what happens in the classical compliment pathway

A

fixation of c1 to antigen-antibody complexes

82
Q

what happens in teh alternative compliment pathway

A

microbe cell wall components combine with plasma proteins (Factors b,d)

83
Q

what happens in the lectin compliment pathway?

A

plasma lectin binds microbial mannose and stimulates classical pathway

84
Q

c3a, c5a results

A

increase vascular permeability and simulate mast cells to release histamine

85
Q

c5a activates what

A

the lipogenous pathway for AA metabolism

86
Q

c5a, c4a, c3a activate?

A

leukocytes - increasing their endothelial adhesion

- also chemotatic agents for neuts, eos, basos, and monos

87
Q

c3b acts as?

A

opsonin for enhanced phagocytosis

88
Q

what is the MAC?

A

essentially multiple C9 proteins (formed by 5b-c9)

- creates pores that violate the membranes of some bacteria

89
Q

most of the time we do not want to activate compliment - so what do we do?

A

inhibitors free within the plasma and associated with cells protect host tissue

  • c1 inhibitor blocks activation of c1
  • decay acclerating factor (DAF) and factor H limit C3/C5 convertase formation
90
Q

coagulation / kinin systems overlap?

A

the cogaulation system overlaps with mediators fo inflammation

91
Q

what is Hageman factor?

A

factor XII is an important clotting factor that activates the kinin system

92
Q

what is the kinin system

A

ultimately system leads to bradykinin which causes increased vascular permeability, vascular dilation, and pain

intermediate product kalikrein is chemotatic and activates factor XII

93
Q

Factor XII (Hageman factor) is an important clotting factor, what does it do?

A

Stimulates the clotting cascade, including several other factors that impact inflammation

94
Q

What other factors does factor XII stimulate that impact inflammation?

A

factor Xa - which lead to vascular permeability

thrombin

95
Q

What does factor Xa do?

A

leads to vascular permeability

96
Q

what does thrombin do (3)

A

binds to protease activated receptors on endothelial cells, activating them

cleaves fibrinogen creating fibrinopeptides which increase vascular permeability and are chemotatic

thrombin cleaves compliment factor 5 forming factor 5a

97
Q

Whenever clotting system is activated, what other system is activated?

A

fibrinolytic
- multiple of these factors are active inflammatory mediators resulting in vascular permeability, dilation, and C3a formation

98
Q

what helps tamp down inflammation?

A

several factors serve to antagonize the driving / facilitating mediators of inflammation

99
Q

what destroys many of the circulating inflammatory mediators?

A

circulating enzymes - that have short active periods

100
Q

what doe lipoxins do?

A

antagonize luekotrienes

101
Q

what do compliment regulatory proteins do?

A

antagonize mediators of inflammation (C1 inhibitor)

102
Q

IL-10 what does it do? where does it come from?

A

secreted by macrophages

down regulates activated macrophages

103
Q

TGF beta

what does it do?

A

promotes fibrosis

is an anti-inflammatory

104
Q

do only extracellular compounds antagonize pro-inflammatory cells?

A

no - intracellular compounds also antagonize pro-inflammatory cell states

Disease and Defense (12 decks)

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