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Immunology > Inflammation 3 > Flashcards

Inflammation 3 Flashcards

1
Q

following invasion by pathogens get

A

immediate response (innate)

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2
Q

innate response starts as soon as

A

pathogen enters

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3
Q

how long does immediate innate response last

A

4 hours

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4
Q

activation of what contributes to immediate innate response

A

adaptive pathway

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5
Q

recognizing pathogen is job of

A

PRR (on epithelial cell, tissue macrophages, mast cells, etc)

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6
Q

immediate innate response will rarely if ever result in

A

elimination of pathogen

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7
Q

innate response will lead to what symptom

A

inflammation

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8
Q

symptos of inflammation

A

fever

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9
Q

macrophages secrete variety of mediators that promote

A

inflammatory response

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10
Q

its possible pathogen may be eliminatedat which first stage

A

PRR and PAMP stage

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11
Q

adaptive response can detect as early as

A

4-5 days

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12
Q

when is adaptie response optimal

A

week after infection

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13
Q

once t cells are generated in secondary lymphoid tissue what will have to do to contact the bad cells

A

go to site of infection

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14
Q

inflammation exists to solve what problem

A

most infection is in tissue
the cells to fight (immune cells) are in circulation
want to get cells to the infected tissue

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15
Q

describe of inflammation

A

vasodilation

more permeability

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16
Q

inflammation can be innitated by

A

immune or non immuen stimulus

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17
Q

first step in Immunological Steps in Inflammation

A

initiation

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18
Q

describe initiation

A

trauma, tissue necrosis, infection or immune reaction

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19
Q

what is second step in Immunological Steps in Inflammation

A

Acute Vascular Phase

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20
Q

crucial for Acute Vascular Phase

A

activation of mast cells

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21
Q

describe Acute Vascular Phase

A

release of vasoactive compounds from mast cells and macrophages leads to endothelial cell contraction and vasodilation and transudate release

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22
Q

if non immune stimulas stop at what stage of step in Immunological Steps in Inflammation

A

stage 3

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23
Q

if immune stimulus continue to what stage after stage 3 for step in Immunological Steps in Inflammation

A

Acute Cellular Phase

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24
Q

describe Acute Cellular Phase

A

Chemotaxis, margination and emigration (transmigration/diapedesis) of neutrophils; diapedesis of erythrocytes. Resolution may occur at this stage if stimulus is adequately removed

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25
Q

chemotaxis is largely reuslt of production of

A

chemokines and other chemoattractants

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26
Q

chemokins promote neutrophils

A

halting on surface of endothelial cells

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27
Q

when leukocytes pull themselves through gaps b/w endothelial cells that step is called

A

diapedesis

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28
Q

neutrophils have to actiely do what thorugh gaps

A

pull themselves through

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29
Q

what is second to last step of Immunological Steps in Inflammation

A

Chronic Cellular Phase

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30
Q

acute dominated by

A

neutorphils

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31
Q

chronic inflammation dminated by

A

mononuclear cells → lymphocytes & monocytes

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32
Q

chronic cellular phase

A

Emigration of lymphocytes, infiltration by macrophage, emigration of eosinophils in parasitic infections or in allergic responses

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33
Q

what is last step in Immunological Steps in Inflammation

A

resolution

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34
Q

many mediators are already profiormed inside

A

mast cells

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35
Q

resolution stage has what two very important cytokines

A

IL 10

TGF beta

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36
Q

IL-10 and TGF beta are what kind of cytokines

A

immunosuppressive
downregulate the inflammatory response
downregulate adaptive immune resopnse

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37
Q

some mediator srelease by mast cells stimulate contractino of

A

endothelial cells - so gap forms b/w endothelial cells

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38
Q

b/w endothelial gaps

A

leukocytes pull through to get to infected tissue

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39
Q

diaphedes of erythorcytes

A

why the infected are becomes red - vasodilation and RBC extravacating from cciruation into infected tissue

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40
Q

what are five cardinal signs of inflammation (or main 4 + fifth if severe)

A 
Rubor – Redness
Tumor – Swelling
Calor – Heat
Dolor – Pain
Functio laesa – Loss of Function (only if severe)
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41
Q

describe the manifestation of signs of inflammation

A

immediate line of vasoconsturction then redness and vasodilation fo capillaries and arterioles. then swelling due to increase in vascular permeability due to endothelial cells pulling apart and fluid passing into the tissue

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42
Q

what is crucial to inflammation

A

mast cells

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43
Q

control of infiltration of inflammatory cells into tissue via

A

mast cells

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44
Q

how to activate mast cells

A

c3a and c5a

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45
Q

c3b and c4b are

A

opsinins

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46
Q

c3b and c4b allow leukocytes to

A

identify what it is they need to get rid of

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47
Q

c5a and c3a increas vascular

A

permeability → more complement proteins getinto complement tissue

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48
Q

bradyknin is main mediator that causes

A

pain

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49
Q

bradyknin induces an increase in

A

vascular permeability

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50
Q

c5a and c3a bind to receptors on mast cells and stimulate them to

A

degranulate - release contents fo their granules

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51
Q

mast cells also have PRR on their surface, so infectious agent by PAMPs binding can stimulate

A

mast cell degranulation

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52
Q

once mast cells stimulated to degranulate they will release

A

lots of pro-inflammatory mediators

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53
Q

what is released by mast cells

A

histamine
TNF alpha
IL-1

54
Q

histamine is stored preformed in

A

mast cells

55
Q

histamine induces

A

vasodilation

increase in vascular permeability

56
Q

affect of histamine is immediate but

A

short lived

57
Q

what induces sustain in vascular permeability

A

TNF alpha and IL-1

58
Q

TNF alpha and IL-1 induce iadhesion

A

on endothelial cells - so endothelial cells are sticky for other neutrophils. now neutrophils can grab on something to halt when they get to site of infection

59
Q

inreas in vascular permeability allows plamsa proteins to seep from

A

cirulcaiton into tissue

60
Q

bradyknin can stimualte degranulation of

A

mast cells

61
Q

mast cells secrete what chemoattractant

A

IL-8 or (CXCL8)

62
Q

all chemoattracts stimulate through

A

heterotrimeric G protein coupled receptors

63
Q

mast cells secrete IL-8 and also release what lipid chemoattractant

A

LTB4

64
Q

what is most potent chemoattractant for neutrophils

A

IL-8

65
Q

mast cells are not the only cells activatied to initate leukocytes what else can be activated

A

activated by PAMPs binding to PRRs

66
Q

activation of macrophages important b/c they are rich source of

A

pro-inflammatory ctokines

67
Q

macrophages make

A 
IL-1
TNF alpha
IL-6
IL-8
IL-12
68
Q

IL-1
TNF alpha
IL-6 control what

A

acute phase response

69
Q

IL-8 is a chemoattratant for

A

neutrophils

70
Q

IL-12 activtes

A

natural killer cells

71
Q

natural killer cells are important for killing spread of

A

viral infections

72
Q

IL-6 is main factor responsible for

A

heat associated with acute inflammation

induces fat and muscle metabolism which riases temp

73
Q

IL-8 is

A

chemoattractant

74
Q

IL-12 activates

A

NK cells

75
Q

features of acute phase response

A

production of proteins importat for inflammation - so it repleneshes what we are using up
bone marrow endothelium - neutrophil mobilization “pus” mobilize the neutrophils from bone marrow and then attracted to site of infection by chemoattractants
hypothalamus - increase in body temp
IL-6 acts on fat and muscle for localized heat

76
Q

mannose-bindin lectin

A

initator of ____ pathway

77
Q

IL-1
TNF alpha
IL-6 are not

A

acute phase proteins, they just stimulate production of acute phase proteins

78
Q

acute phase proteins also called

A

acute phase reactant

79
Q

main function of acute phase response

A

replenishes what we are using up - like complement and neutrophils

80
Q

acute phase response is regulated by

A

IL-1 IL-6 TNF alpha

81
Q

IL-1 IL-6 TNF alpha act where

A

locally and distally - from bone marrow to hypothalamus to liver

82
Q

acute phase proteins can limit

A

damage

83
Q

name a very important representative of acute phase proteins

A

CRP (C reactive protein)

84
Q

why are acute phase proteins important

A

cell surface or soluble PRRs
can measure them to get indication of repsonse to treatment
they will change their plasma concentration if there is inflammation or trauma going on

85
Q

list the important acute-phase proteins

A

pg 66

86
Q

suspect infection what test would you request

A

plasma or serum c-reactive protein

87
Q

with activation of mast cells and release of chemoattractants calling out for

A

leukocytes - particarlly neutrophils

88
Q

for neutrophils to get to infection

A

have to leave circulation and get to tissue

89
Q

to get leukocytes migration need

A

chemoattractants

90
Q

formylated peptides are characteristic of

A

bacteria

91
Q

n-formlyated baterial peptides do what

A

chemoattractant

92
Q

example chemoattractants to get leukocytes to site of infection

A 
Examples:
N-Formylated bacterial peptides – FMLP
Complement derived – C5a, C3a
Lipid derived – Leukotriene B4 (LTB4)
Chemoattractant cytokines
Chemokines
e.g. - IL-8 (CXCL8), CCL5, CCL21
93
Q

following exposure to chemoattract the leukocyte will migrate

A

to where the chemoattract is in highest concentration

94
Q

chemotaxas

A

moving up the chemoattractant gradient

95
Q

chemoattractans will stimluate what in neutrophil

A

to destory the pathogen once it takes it up

96
Q

all chemoattracts ibnd to

A

7 pass membrane g protein coupled receptors

97
Q

exposure of the neutrophil to chemoattractants results in increase in what

A

affinity of integrin for contrareceptor

98
Q

four main families of chemokines

A

CXC chemokines
CC chemokines
(X)C chemokine
CX3C chemokine

99
Q

chemokines classified on arrangement of

A

conservedn terminal cystein

100
Q

CC chemokines have no intervening what the cysteins

A

no intervening aa

101
Q

what is the clinical significance of chemokines in regards to HIV

A

CCR5 (M strain) CXCR4 (T strain)

102
Q

chemokine receptors can bind more than one

A

chemokine

103
Q

there is no numerical correlation b/w chemokine and

A

chemokine receptor - there is no correlation b/w what they bind to

104
Q

single chemokine can bind to multiple

A

receptors

105
Q

all chemokine receptors are

A

7 pass transmembrane g protein coupled receptors

106
Q

for neutorphils to get from ciruclation into tissue have to do w=somethign to blood vessel endothelial cells, they have to adhere, the initial adherence is a very

A

low infinity interaction

107
Q

the first reaction to endothelial cells is not sufficient

A

to stop neturophils b/c its so weak

108
Q

normally endothelial cells are non inflamed and its not

A

sticky for neutrophils

109
Q

during inflammation it induces expression of adhesion molecules onto

A

neutrophils - the endothelial cells slow down neutrophils

110
Q

first cell into site of infection is

A

neutrophil

111
Q

dominant leukocyte we have

A

neutrophil

112
Q

four types of adhesion molecules to regulate immune cell intearaction to get to site of infection

A

addressins CD34
selectins - L-selectin
integrins - LFA-1
immunoglobulin like - ICAM-1

113
Q

inital low affinity interactions of neutrophil and endothelial wall are b/w

A

addressins & selectins

114
Q

when leukocytes arrive they will roll along surface of endothelial cells this is called

A

margination

115
Q

rolling of leukocyte cell in cirulation is due to interaction b/w

A

adressin and selectins

116
Q

adressin and selection interaction is not sufficient affinity to

A

bring neutrophil to a halt

117
Q

what interaction brings neutrophil to a halt

A

integrin (LFA-1) and ICAM-1

118
Q

when neutorphil arrives to ICAM-1 and binds the interaction isn’t strong enough to get it through the endothelial cells - it then binds to CXCL8 and enduces

A

conformational change in LFA-1 to neutrophil and beocmes high affinity. the high affinity state is responsible for bringing neutrophil to halt on surface of endothelial cells

119
Q

PECAM1 is located where

A

at junctions of individual endothelial cells

120
Q

binding of neutrophils to PECAM-1 pulls it through the gaps of endothelial cells. ligand for PECAM-1 is

A

PECAM-1

121
Q

once neutrophil comes to a haltthey will use what to pull them across the endothelial cell layer

A

PECAM-1

122
Q

describe the 4 step model of extravastion of elukocyte into tissue

A

pg 81

123
Q

diapedesis is what

A

crossing of blood vessel wall

124
Q

by who and when are IL10 and TGF beta produced?

A

by macrophages

produced towards end of inflammatory response

125
Q

what are prostaglandins

A

lipid mediator that induces vasodilation

126
Q

CXC chemokines strucrure

A

an aa b/w two cycsteins

127
Q

(X)C chemokine structures

A

a single cys

128
Q

CX3C chemokine structure

A

Cys-X-X-X-Cys

129
Q

LFA-1 binds to

A

ICAM-1

130
Q

what interaction brings the neutrophil to a halt

A

LFA-1 binding to ICAM-1

131
Q

where is L selectin located

A

on neutrophil

Immunology (12 decks)

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