Immunity system Vs Pathogens L16 Flashcards

1
Q

what is a microbiome

A

microbial communities of tissues (skin, oral mucosa, gastrointestinal tract)

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2
Q

effect of microbiome

A

cause no damage to host, can perform important functions

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3
Q

are different microbiomes recognised

A

Immune system must be able to recognise difference

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4
Q

what cells are humans mainly made of

A

more prokaryotic than eukaryotic cells

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5
Q

when do commensals become pathogens

A

when in the wrong location

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6
Q

what is the difference between pathogens and commensals

A

whether they cause damage

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7
Q

what is the distribution of PRRs

A

have more effect on pathogens and less effect on commensals

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8
Q

what are the cell surface receptors

A

toll-like receptors

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9
Q

what are the pathogenic factors

A

virulence factors so they can attach/invade (NLR’s)

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10
Q

what are indigenous microbiota like

A

non-invasive

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11
Q

what do commensals interact with

A

only apical surface TLRs

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12
Q

what does the microbiome do

A

evolved to lessen inflammation

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13
Q

what is on the apical surface

A

Microbiome on apical surface of villi – microvilli

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14
Q

what happens when invasion occurs in mucosa

A

invading come into contact with cytosolic NLR’s

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15
Q

what are the TLRs like on the apical surface compared to basolateral

A

TLR’s on apical surface are less responsive than ones on host basolateral side of epithelial cells

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16
Q

where do commensals interact with

A

less responsive apical side

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17
Q

how is inflammation lessened

A

by dampening epithelial cell TLR signalling

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18
Q

what is the mucosal immune system

A

area of an intestinal villus
mucosal immunity functions independently of regional lymph nodes to control inflammation induced by microbiota or to stimulate

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19
Q

what are IECs

A

intestinal epithelial cells

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20
Q

what respiration do bacteria have

A

anaerobic and aerobic

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21
Q

what shape are bacteria

A

cocci and bacilli

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22
Q

what gram are bacteria

A

gram-positive

gram-negative

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23
Q

what is a capsule

A

protects against phagocytosis

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24
Q

what do bacteria contain

A

toxins

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25
Q

what are flagella for

A

attachment
motility
injection needle

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26
Q

how are flagella used as injection needle

A

allows bacterial factors to come into the host cell through end of the flagella

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27
Q

what is bacteria attachment for

A

help attach bacteria to the surface

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28
Q

how does phagocytosis work against bacteria

A

Host immune cell recognises the bacteria, engulfs it and breaks it down in phagolysosome

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29
Q

how does bacteria counter phagocytosis

A

covers self in capsule so isn’t recognised

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30
Q

what do antibodies do to help against bacteria

A

immune system has an antibody that recognises the capsule so can be taken up by macrophage/neutrophil
prevent toxins entering cell

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31
Q

what does the complement assist

A

phagocytosis and enhances inflammation

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32
Q

what do helper T cells activate

A

activate macrophage to kill intracellular bacteria in MHC recognition

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33
Q

what do cytotoxic T cells kill

A

kill infected host cells and activated macrophages

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34
Q

how does bacteria escape phagosome

A

using hemolysins

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35
Q

how does phagosome-lysosome fusion become inhibited

A

secreting proteins into host cytosol, which interfere with the signalling pathways that cause the fusion

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36
Q

what does bacterial evasion induce

A

Induce production of anti-inflammatory cytokines

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37
Q

what is inhibited by bacterial evasion

A

Inhibit signal transduction of proinflammatory cytokines

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38
Q

what is expressed in bacterial evasion

A

Express proteins that can cause apoptosis of T cells

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39
Q

what happens after pathogen escapes phagosome

A

the host cells can form an autophagosome

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40
Q

what is the immune system like

A

highly regulated mechanism

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41
Q

what is delivered in immune system

A

intracellular pathogen to lysosomes

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42
Q

what is one of the most common causes of gastroenteritis in the world

A

Campylobacter jejuni

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43
Q

what is Campylobacter jejuni characterised by

A

abdominal pain, fever and diarrhoea

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44
Q

what is the flagella of Campylobacter jejuni important for

A

colonisation

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45
Q

what happens if Campylobacter jejuni

invasion

A

Invasion of host cells activates production of cytokines

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46
Q

what is sialylation

A

addition of sialic acid groups onto oligosaccharides

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47
Q

what is LOS

A

Lipooligosaccharides

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48
Q

what can flagella be used as in Campylobacter jejuni

A

can be used to as an apparatus to secrete proteins such as Campylobacter invasion antigen (cia)

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49
Q

what is GBS

A

Guillain-Barré Syndrome

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50
Q

what does LOS do

A

mimic structure of human gangliosides (molecular mimicry)

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51
Q

what can antibodies against the C. jejuni LOS lead to

A

autoimmune response, resulting in Guillain-Barré Syndrome

52
Q

is GBS fatal

A

can be fatal

53
Q

what are the symptoms of GBS

A

vary from mild muscle weakness to potential paralysis

54
Q

what is CDI

A

Clostridium difficile infection

55
Q

what does clostridium difficile toxins cause

A

cause severe inflammatory reaction leading to microulcerations

56
Q

what are the two main toxins of Clostridium difficile

A

TcdA and TcdB

57
Q

what are the toxins like that clostridium difficile secrete

A

Large secreted proteins

58
Q

what do clostridium difficile toxins interact with

A

epithelium cause inflammatory response

59
Q

what is SLP

A

surface layer proteins

60
Q

what does TcdA cause

A

apoptosis in monocytes

61
Q

what is SLP like

A

highly variable across different strains, may have role on evasion of host immune response

62
Q

where are defensins secreted

A

by specialist cells in intestinal epithelia, can reduce tissue damage due to toxins

63
Q

what do defensins do

A

reduce inflammatory cytokine production, thereby regulating the immune response

64
Q

what is staph aureus

A

Common human pathogen; component of the commensal flora and major cause of invasive infection

65
Q

what us staph aureus responsible for

A

majority of skin and soft tissue infections in humans

66
Q

what can staph aurea cause

A

invasive and life-threatening infections

67
Q

what is the problem with the treatment of staph aureus

A

complicated by the emergence of methicillin-resistant S. aureus (MRSA) strains, which are becoming increasingly resistant to multiple antibiotics

68
Q

what does staph aureus interfere with

A

innate immune response

69
Q

what does staph aureus express

A

wide variety of virulence factors

Expresses SpA protein

70
Q

what does SpA protein that staph aureus expresses cause

A

binds to antibodies and prevents opsonophagocytic killing

71
Q

what is needed to clear staph aureus

A

neutrophils

72
Q

what are NETs

A

neutrophil extracellular traps

73
Q

what are NETs made of

A

comprised of DNA and antimicrobial peptides

74
Q

what do antibodies do to viruses

A

Antibody blocks ability of virus to invade cells

75
Q

how do antibodies prevent virus entry into cell

A

Antibody recognizes the PAMPs and virus cant get into the cell

76
Q

what happens to cell surface if infected

A

MHC class 1, if infected can express peptides on surface of that pathogen

77
Q

what happens if MHC class 1 on cell surface

A

Cytotoxic lymphocytes can recognise and kill the pathogen

78
Q

if no expression of MHC class 1 what happens

A

natural killer cells compensate, recognise no MHC class 1 on surface so has to kill cell

79
Q

what do viruses do to prevent MHC class 1 on surface

A

avoid NK cells recognition viruses can display a decoy MHC I-like molecule on cell surface (human cytomegalovirus)

80
Q

what do viruses do to down regulate MHC

A

viruses make proteins that down regulate MHC class I molecules on infected host cell surface

81
Q

what do tetherin act against

A

enveloped viruses

82
Q

where does tetherin bind to

A

Binds to the surface glycoproteins

83
Q

what do tetherin act against

A

Act against a wide range of viruses (retroviruses; ebolaviruses)

84
Q

what does tetherin prevent

A

release of the virus while budding

Retained particles are targeted for degradation

85
Q

what does tetherin trigger

A

inflammation

86
Q

what is CMV

A

cytomegalovirus

87
Q

what is Vpu

A

viral protein U

88
Q

how is tetherin degraded

A

HIV expresses Vpu, which triggers degradation of Tetherin

89
Q

what is tetherin co-opted for

A

entry pathway of CMV

90
Q

what does ebola glycoprotein inhibit

A

inhibits Tetherin association with a viral surface protein

91
Q

what can yeast be

A

filament

yeast

92
Q

what does the immune system recognise in fungi

A

cell wall

93
Q

what is fungi part of

A

commensal flora

94
Q

what can fungi cause

A

infection in absence of an effective immune response

95
Q

what do dendritic cells do to fungi

A

phagocytose fungal cells

96
Q

what peptides are expressed in relation to fungi

A

MHC class 2

97
Q

what is required for effective immune response against C. albicans

A

Both CD4 and CD8 T cell

98
Q

how are T cells activated

A

Need the peptides to be presented by MHC class II on dendritic cells to get activation of T cell response

99
Q

effect of CD8 T cells on fungi

A

CD8 T cells been shown to inhibit fungal cell growth

100
Q

what can help clear fungi infection

A

innate immune system

101
Q

what are the main four divisions of protozoa

A

flagellates
amoebas
ciliates
sporozoa

102
Q

what causes malaria

A

Plasmodium falciparum

103
Q

where do plasmodium falciparum replicate

A

can only replicate in erythrocyte

104
Q

effect of antibodies on Plasmodium falciparum

A

can inhibit uptake into erythrocytes and hepatocytes

105
Q

how does erythrocytes differ

A

Erythrocytes naturally don’t have MHC class I on surface (un-nucleated cells)

106
Q

effect of Plasmodium falciparum

A

down regulate T helper cytokines

107
Q

what is virulence mainly associated with

A

immune evasion

108
Q

what are polymorphic proteins

A

immunologically distinct

109
Q

what does Plasmodium falciparum cause

A

highly polymorphic surface proteins

110
Q

what is there a lack of in Plasmodium falciparum

A

Lack of MHC class I on RBC’s protect from CD8 T cells

111
Q

What are the immune attack

A

Opsonising antibodies
Complement deposition
Invasion blocking antibodies

112
Q

What does opsonising antibodies lead to

A

Phagocytosis

113
Q

What does complement deposition lead to

A

Phagocytosis

Lysis

114
Q

What are the immune evasion strategies

A

Varying sequence while maintaining function
Redundancy in multi-gene families
Reduced antigenicity

115
Q

what is trypanosomiasis

A

sleeping sickness

116
Q

what is trypanosma brucei like

A

extracellular

117
Q

what protects against trypanosma brucei

A

Variant surface proteins to protect from immune system

118
Q

what can dampen inflammatory response

A

Saliva from infected tsetse fly

119
Q

what are helminths

A

Worms that live like parasites

120
Q

what are helminths like

A

Mostly extracellular, move to organs

121
Q

what is the immune system problem with helminths

A

cannot phagocytose them

122
Q

what are the symptoms of Schistosoma mansoni

A

Diarrhoea, blood in faeces, organ damage

123
Q

what is Schistosoma mansoni associated with

A

chronic (long term) disease

124
Q

what does Schistosoma mansoni have to protect against

A

both eggs and adult worms

125
Q

what does Schistosoma mansoni cause

A

Venous blood release of eggs into environment

Granuloma formation to contain eggs