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Block 6 Week 1 > Innate Immunity- Hunter > Flashcards

Innate Immunity- Hunter Flashcards

1
Q

What are these a part of:
epithelial barriers
anti-microbial enzymes and peptides
the complement system
macrophages, dendritic cells, and neutrophils (myeloid cells)
patter recognition receptors that are germline encoded
inflammation (rubor, calor, tumor, and dolor)
cytokines, chemokines, adhesion molecules, and acute phase proteins
interferons and NK cells

A

Innate immunity (first line of defense)

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2
Q

What does it mean to be colonized by a microbe?

A

you have an organism that is on or in your tissues but barriers have not been perturbed and therefore there is not immune response

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3
Q

What does it mans to be infected by a microbe?

A

An organism has penetrated you tissues but the response is subclinical (not presenting readily observable symptoms)

NOTEdisease has observable symptoms**

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4
Q

What is this:

a pathogen that resides on or in the body but causes disease only when the host is immunosuppressed.

A

opportunistic pathogen

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5
Q

What are three sources of pathogens?

A

environmnt
humans
animals (zoonotic diseases)

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6
Q

What is the mode of transmission to be infected by a pathogen in the airways?

A

inhaled droplets and spores

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7
Q

What pathogen can you get by inhalin a droplet and pentrating the mucosal surface of your airway?
What does this cause?

A

influenze virus

influenza

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8
Q

What pathogen can you get via spores that pentrate the mucosal surface of your airway?
What does this cause?

A

neisseria meningitidis->meningococcal meningitis

bacillus anthracis-> inhalation anthrax

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9
Q

What is the mode of transmittion to infect the GI tract?

A

comtainated food or water

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10
Q

What pathogen can you get by eating or drinking contaminated food or water?
What does this cause?

A

salmonella typhi-> typhoid fever

rotavrius-> diarrhea

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11
Q

What is the mode of transmission to infect the reproductive tract?

A

physical contact

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12
Q

What pathogen can you get through physical contact that will affect your reproductive tract?
What does this cause?

A

treponema pallidum-> syphilis

HIV-> AIDS

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13
Q

What are the three mucosal surfaces that are suscpetible to pathogens?

A

airway
GI Tract
Reproductive Tract

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14
Q

What are the three routes of entry into your external epithelia?

A

external surface
wounds and abrasions
insect bites

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15
Q

What is the mode of transmission to infect your external surface?

A

physical contact

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16
Q

What pathogen can you get through physical contact that will affect your external surfae?
What will this cause?

A

trichophyton-> athlete’s foot

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17
Q

What is the mode of transmission to infect wounds and abrasions?

A

minor skin abrasions
puncture wounds
handling infected animals

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18
Q

What pathogen can you get through minor skin abrasions?

What does this cause?

A

bacillus anthracis-> cutaneous anhrax

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19
Q

What pathogen can you get through puncture wounds?

What does this cause?

A

clostridium tetani-> tetanus

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20
Q

What pathogen can you get through handling infected animals?
What does this cause?

A

francisella tularensis-> tularemia

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21
Q

What type of insect bites can infect your external epithelia?

A 
mosquito bites (aedes aegypt)
deer tick bites
mosquito bites (anopheles)
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22
Q

What pathogen can you get through mosquito bites (aedes aegypti)
What does this cause?

A

flavivirus-> yellow fever

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23
Q

What pathogen can you get through deer tick bites?

What does this cause?

A

barrelia burgdorferi-> lyme disease

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24
Q

What pathogen can you get through mosquito bites (anopheles)?
What does this cause?

A

pasmodium spp. -> malaria

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25
Q

Do all organisms have to penetrate tissues to cause sickness?

A

no (think cholera)

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26
Q

If you have an aborgated immune response such as AIDS or malnutrition, what are these people susceptible to?

A

opportunistic pathogens

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27
Q

the immune system is assisted by what three kinds of barriers?

A

Mechanical
chemical
microbioloical

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28
Q 
What kind of barriers are these:
longitudinal flow of air or fluids
movement of mucus by cilia
tears
nasal cilia
EPITHELIAL TIGHT JUNCTIONS
A

mechanical barriers

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29
Q

What kind of barriers these:

fatty acids, Beta defensins, lamellar bodies, cathelicidin

A

chemical barriers for the skin

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30
Q

What kind of barriers are these:

low ph, enzymes (pepsin), alpha-defensins (cryptdins), regIII (lecticidins), Cathelicidin

A

chemical barriers for the gut

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31
Q

What kinds of barriers are these:

pulmonary surfactant, alpha densins, cathelicidin

A

chemical barriers for the lungs

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32
Q

What kinds of barriers are these:

enzymes in tears and saliva (lysozyme), histatins, beta defensins

A

chemical barriers for eyes/nose/oral cavity

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33
Q

What is the microbiological barriers for the skin, gut, lungs, eyes/nose and oral cavity?

A

normal microbiota

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34
Q

endotoxins are caused by what kind of bacteria?

A

gram negative

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35
Q

Vibrio cholera, strep and staph are all what kind of toxin?

A

exotoxin (meaning they release toxins to allow for the penetration of tissues)

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36
Q

E. Coli, salmonella are what kind of toxin?

A

endotoxins (a toxin that is present inside a bacterial cell and is released when the cell disintegrates. It is sometimes responsible for the characteristic symptoms of a disease)

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37
Q

AN endotoxin has a lipopolyscharide toxin found in the (blank) of the organism and will perturb the immune system in massive ways by triggering a bunch of cytokines and a over active immune response

A

cell wall

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38
Q

What kind of mechanism is this: a pathogen gets inside a cell and uses the cells machinery and then destroys the cell and moves on to a new one

A

direct cytopathic effect

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39
Q

What do you call a direct mechanism of tissue damage by pathogens?

A

microbial pathogenesis

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40
Q

What do you call indirect mechanisms of tissue damage by pathogens?

A

immunopathology

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41
Q

What are the three pathogenic mechanisms that cause direct tissue damage?

A

exotoxin production, endotoxins, and direct cytopathic effects

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42
Q

What are immune complexes?

A

It’s when really large antibodies attach to antigens and then you cant get them filitered out of your body
(they get stuck places like blood clots)

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43
Q

What are anti-host antibodies?

A

When your body makes antibodies that attack the self

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44
Q

What are the three types of anti-microbial enzymes?

A

lysozyme
pepsin
secretory phospholipase A2

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45
Q

How does lysozyme work?

A

it chews up the outer petidoglycan layer of the cell wall of gram-positive bacteria.

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46
Q

Do gram positive bacteria and gram negative bacteria have the same type of cell wall?

A

no

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47
Q

Do both gram positive and gram negative bacteria have peptidoglycan layers in their cell wall?

A

yes

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48
Q

Which type of bacteria has teichoic acid and lipteichoic acid, gram negative or gram positive bacteria?

A

gram-positive bacteria

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49
Q

What are the four major classes of anti-microbial peptides?

A

defensins alpha
defensins beta
cathelicidins
histatins

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50
Q

Are anti-microbial peptides, short or long?

A

short

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51
Q

Anti-microbial peptides are activated by proteolysis to relases (blank) peptides

A

amphipathic

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52
Q

How do defensins work?

A

They have a positive charge on one side and a hydrophobic charge on the other which will allow them to enter the lipid membrane and create a pore in the microbial membrane.

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53
Q

How do you make an anti-microbial protein?

A

they are pro hormones that are cleaved into an active form

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54
Q

Are antimicrobial proteins a primary or secondary defense

A

primary defense

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55
Q

Pathogens that breach epithelial barriers encounter (blank) that trigger (blank)

A

Macrophages

inflammation

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56
Q

How do macrophages recognize pathogens?

A

by genome encoded receptors (e.g TLRs)

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57
Q

(blank) cause vasodilation, increased vascular permeability, and upregulate expression of adhesion molecules on endothelium

A

cytokines (e.g TNF-alpha)

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58
Q

Activation of the (blank) and (blank) systems cause pain and blood clotting

A

kinin and coagulation systems

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59
Q

(blank) attract neutrophils (CXCL8) and monocytes as a second line of defense

A

chemokines

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60
Q

(blank) an (blank) componenets like complement engage the pathogens and often eliminate them before an adaptive immune response is generated.

A

phagocytic cells and plasma components

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61
Q

What is the most important component of adaptive immunity?

A

inflammation

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62
Q

How do macrophages trigger inflammation?

A

they trigger cytokines and chemokines, neutrophils and more macrophages

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63
Q

What is sepsis?

A

when the inflammatory process gets out of hand (release of massive amounts of cytokines and you have too high of permeability in your vascularization)

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64
Q

What is the most important pro-inflammatory cytokine that causes vasodilation and vascular permeability?

A

TNF alpha

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65
Q

After macrophages tell cytokines to come to the tissues, what do they call next to come help?

A

neutrophils and other macrophages

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66
Q

Which or the stronger phagocytic cells, macrophages or neutrophils?

A

neutrophils

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67
Q

What do macrophages recognize?

A

pathogen associate molecular patterns

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68
Q

Can macrophages recognize common motifs? what is a very common one?

A

yes

peptidoglycan

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69
Q

What do macrophages recognize easily on gram-positive bacteria?

A

peptidoglycan

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70
Q

What do macrophages easily recognize on gram-negative bacteria?

A

Lipopolysaccharide (LPS)

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71
Q

What does endotoxin bind to?

A

Toll receptors (TLR

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72
Q

What are recognized by their motif F-Met-Leu-Phe?

A

bacteria

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73
Q

What carry mannose receptors?

A

bacteria, fungi, viruses

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74
Q

What carry scavenger receptors?

A

acetylated lipoproteins on bacteria

75
Q

What carry dectin-1 glucan receptors?

A

fungi

76
Q

What carry LPS binding proteins, TLR-4 and CD14?

A

gram negative bacteria

77
Q

What are Toll-Like Receptors?

A

pathogen recognition and signaling molecules

78
Q

How many human TLR genes are there?

A

10

79
Q

TLR proteins are (blank) receptors

A

PAMP (pathoen associated molecular patterns)

80
Q

TLR 5 evolved to recognize what?

A

flagelin

81
Q

You can find (blank) inside vacuoles inside of macrophages.

A

TLR

82
Q

In innate immunity (blank) have evovled to create the initial self-non self discrimination of the immune system.

A

TLR Receptors

83
Q

Where do you find TLR receptors?

A

on the cell surface and intracellularly

84
Q

TLR activation engages the transcription factor (blank) and induces the production of inflammatory mediators.

A

NF-kB

85
Q

(blank) are similar in structure to TLR, detect cytoplasmic bacteria, and signal inflammation

A

Nucleoside Oligomerization Domain (NOD)-like proteins

86
Q

(blank) detect viral RNA in the cytoplasm and signal inflammation

A

retinoic acid inducible gene -I

(RIG)-like proteins

87
Q

What does TLR 2 and TLR 6 recognize?

A

diacyl lipopeptides

88
Q

what does TLR2 and TLR1 recognize?

A

triacyl lipoproteins

89
Q

What does TLR-4 recognize?

A

LPS

90
Q

What does TLR 3 recgonize?

A

dsRNA

91
Q

What does TLR7 recognize?

A

ssRNA

92
Q

What does TLR-9 recognize?

A

CpG DNA

93
Q

Where do you find NOD proteins? What do they do?

A

in the cytoplasm

intiate inflammation

94
Q

What do RIG do?

A

detect viral DNA

95
Q

TLR signaling induces (blank)

A

gene transcription

96
Q

Give a brief description of how TLR signaling induces gene transcription

A

PAMP allows for dimerization of TLR which induces intracellular signaling and the gene expression of the transcription factors and cytokines like NF-Kb

97
Q

What is IRAK4?

A

a danger signal

98
Q

What happns when you dimerize TLR receptors?

A

you recruit IRAK1 and IRAK4 to create an immune response

99
Q

IRAK-1 deficiency is a rare autosomal (blank) defect.

A

recessive

100
Q 
What is this:
any of a class of proteins present in the serum and cells of the immune system, that function as antibodies
A

immunoglobulin

101
Q

In detail explain how TLR induces gene transcription

A

Dimierized TLR-> recruits IRAk1 and IRAK4-> IRAK1 and IRAK4 activate E3 ubiquiting ligase Traf-6-> Traf 6 and NEMO are polyubiquitinated-> create scaffolding-> TAK1 gets together with IKK and phosphorylates IKKB which phsophorlates IKB-> IKB degrades-> releases NFkB into the nucleus to induce expression of cytokine genes-> inflammation

102
Q

What is this:

involving or relating to the production of pus.

A

pyogenic

103
Q

The (blank) pathway involves the expression of more than 100 genes

A

NF-kB

104
Q

What are the two major defects in intracellular killing in neutrophils?

A

abnormal respiratory burst

granule abnormalities

105
Q

What are the two types of abnormal respiratory bursts in neutrophil function?

A

chronic granulomatous disease

glucose-6-phosphate dehydrogenase deficiency

106
Q

What are the three types of granule abnormalities in neutrophil function?

A

myeloperoxidase deficiency
specific granule deficiency
chediak-higashi syndrome

107
Q

What is the major defect in adhesion defects in neutrophils

A

leukocyte adhesion deficiency

108
Q

What are the two types of adhesions defects in neutrophils?

A

Type 1, integrin deficiency

Type 2, E-selectin ligand deficiency

109
Q

What is the most important means of defense against extracellular bacteria, fungi and protozoan parasites?

A

phagocytosis and intracellular killing

110
Q

What are the 2 most important phagocytic cells?

A

neutrophils and macrophages

111
Q

Invagination of cell membrane creates the (blank)

A

phagosome

112
Q

(blank) filled with antimicrobial substances fuse with phagosomes and create (blank). This is where most microbes are killed and digested

A

lysosomes

phagolysosome

113
Q

Assembly of the (blank) promotes intracellular microbial killing

A

NADPH oxidase

114
Q

How do you assemble the NADPH oxidase component in the phagolysosomal membrane?

A

microbe phagocytosis and G-protein receptor signaling

115
Q

What does NADPH oxidase generate?

A

antimicrobial superoxide, hydrogen peroxide and other reactive oxygen species (‘respiratory burst”)

116
Q

How do you activate acid hydrolases and antimicrobial peptides within the phagolysosome so that it can kill microbes?

A

lower the pH

117
Q

What does the C5a complement do?

A

augments phagocytosis (internalization and causes formation of NADPH oxidase)

118
Q

What do these make up:

p67, P10, P17, P22, Gp91

A

NADPH oxidase

119
Q

What happens if you have defect in Gp91 and how does it happen?

A

you cant make NADPH oxidase and therefore cannot destroy microbes…. Can be caused by X-linked defects

120
Q

What is respiratory burst?

A

the production of oxygen species via NADPH

121
Q

WHat all can you find within a phagolysosome?

A

acid, toxic oxygen species, NO, antimicrobial peptides (cathelicidn, defensins etc.), enzymes, competitors (lactoferrin)

122
Q

What makes lactoferrin and vit B12?

A

neutrophils

123
Q

What does lysozyme do?

A

digests cell walls of some gram-positive bacteria

124
Q

Why do granulomas form?

A

when the immune system cant get rid of something

125
Q

If you cant reduce dihydrorhodamine, what is the problem?

A

gp91 deficiency and a failed NADPH oxidase system resulting in granulomas or chronic granulomatous disease

126
Q

(blank) lesions in the skin and various internal organs are caused by pyogenic bacteria and fungi

A

Granulomatous

127
Q

What is pyoderma?

A

an infection of the skin (all over the outside of the skin)

128
Q

When your lymph nodes interact with microbes they become (blank)

A

hyperplastic

129
Q

What is the defect in chediak-higashi syndrome and what will you see?

A

defect in microtuble polymerization (decreases phagolysosomes)
recurrent pyogenic infections, partial albinism, large lysosomal vesicles in neutrophils and eosinophils

130
Q

What is neutropenia?

A

you have a low level of neutrophils

131
Q

What are the two ways you can get neutropenia?

A

acquired (common) and hereditary (rare)

132
Q

What are the 2 ways you can get acquired (common) neutropenia?

A

drug-induced (especially cytotoxic drugs for cancer)

autoimmune (anti-neutrophil antibodies)

133
Q

What are three types of hereditary (rare) ways to get neutropenia?

A

familial (benign, ethnic) neutropenia
infantile genetic agranulocytosis (severe congenital neutropenia)
cyclic neytropenia

134
Q

T or F

neutropenia induced by cytotoxic anti-cancer drugs is common

A

T

135
Q

Define neutropenia in terms of cell count

A

1500 to 2000 cells/mm cubed of blood

136
Q

At what neutrophil count to you have an increase in infections?

A

below 1500 cells/mm cubed

137
Q

What are the most common pathogens that take advantage of neutropenia?

A

staph, gram negative bacteria, other encapsulated bacteria, fungi

138
Q

Nearly 15% of sepsis cases are caused by (blank)

A

candida albicans

139
Q

Neutropenic sepsis can be caused by a variety of (blank)

A

pyogenic bacteria and fungi

140
Q

How do you get rid of drug-induced neutropenia?

A

broad-spectrum antibiotics and human recombinant granulocyte colony stimulating factor (hrG-CSF) before subsequent rounds of chemotherapy (increases output of granulocytes of bone marrow)

141
Q

(blank) is a genetically and phenotypically heterogenous group of nehreditary neutropenias seen in infants

A

severe congenital neutropenia (Kostmann disease)

142
Q

What does this describe:
patients present with recurrent infections of skin, soft tissues, lungs and deep organs; sepsis is common, ANC is often below 200/ uL. Differentials includes a wide variety of conditions that impair myelopoiesis. A diagnosis is supported by characteristic findings of maturation arrent at the promelocyte or myelocyte stage.

A

sever congenital neutropenia (kostmann Disease)

143
Q

How do you treat Kostmann disease (severe congenital neutropenia)

A

rhG-CSF or bone marrow transplant

144
Q

What is risky about rhG-CSF?

A

myelodysplasia (refers to a group of disorders in which the bone marrow does not function normally and produces insufficient number of normal blood cells.)
and acute myeloid leukemia (abnormal leukocyte production)

145
Q

What is the chemokine that macrophages use to call in the neutrophils if they cant handle themselves in the tissues?

A

CXCL8

146
Q

Explain how you can get a neutrophil to diapedis across the basement mebrane into a tissue?

A

Neutrophils will roll along the basement membrane until they reach a place of inflammation where they will connect their integrin called LFA1 with its special CD18 component to the ICAM1 adhesion molecule on the basement membrane which will pull it through the cracks of the basememnt membrane

147
Q

What is ICAM-1?

A

it is an immunoglobulin-like molecule that works as an adhesion molecule

148
Q

What is an immunoglobulin?

A

any of a class of proteins present in the serum and cells of the immune system, that function as antibodies.

149
Q

What is CD18?

A

a special component of the integrin LFA1 that is found on neutrophils

150
Q

What is LFA-1?

A

the integrin found on neutrophils that binds to ICAM-1

151
Q

WHat is a rare autosomal recessive disorder presenting with recurrent bacterial infections due to defects in neutrophil adhesion?

A

leukocyte adhesion deficiency (type I)

152
Q

What will adhesion molecule defects result in?

A

poor neutrophil chemotaxis, phagocytosis, neutrophilia (too many neutrophils in thie blood because they are stuck and cant get into the tissues)

153
Q

Infants who have (blank) will suffer from infections such as omphalitis, pneumonia, ginigivitis, and peritonitis

A

leukocyte adhesion deficiency (type I)

154
Q

What is the defect in leukocyte adhesion deficiency type I?

A

beta-2 integrin subunit CDI8

155
Q

How do you determine if someone has leukocyte adhesion deficiency (type I)?
How do you treat it?

A

you look at CD18 levels

bone marrow transplant

156
Q

The acute phase responses is mediated by (blank)

A

acute phase proteins

157
Q

Bacteria induce macrophages to produce (blank), which acts on hepatocytes to induce synthesis of acute-phase proteins.

A

IL-6

158
Q

What is this:
an antibody or other substance that binds to foreign microorganisms or cells, making them more susceptible to phagocytosis.

A

opsonin

159
Q

(blank) is an opsonin and is used to identify patients with active inflammatory processes

A

c reactive protein

160
Q

(blank) binds and sequesters iron to inhibit microbial growth

A

ferritin

161
Q

(blank) is a coagulation factors, its levels correlate w/ erythrocyte sedimentation rate (ESR), an inflammation indicator

A

fibrinogen

162
Q

(blank) production is downregulated during acute phase response.

A

albumin

163
Q

What all are involved in the acute phase response induced by IL6?

A 
C-reactive protein (CRP)
ferritin
fibrinogen
albumin
mannose-bindin lectin
164
Q

What does mannose-binding lectin do?

A

it is an opsonin that activates complements

165
Q

Where does IL6 bind?

A

the liver

166
Q

Viral RNA induces (blank) gene expression

A

interferon alpha/beta (a protein that inhibits virus replication)

167
Q

How does Viral RNA induce interferon gene expression in an endosome?

A

in an endosome TLR3 recognizes viral DNA and recruits TRIF which recruits IRF3 and IRF7 to induce gene expression

168
Q

How does viral RNA induce interferon gene expression in the cytosol?

A

MDA5, RIG-I, CARDIF get together and recruit IRF3 and IRF7 to induce gene expression

169
Q

How do antiviral type I interferons work?

A

an infected cell is recognizesby plasmacytoid dendritic cells that produce large amounts of interferon which will induce the interferon response

170
Q

What is the interferon response?

A

stops virus from replicatng

increases expression of ligands for receptors on NK cells, activates NK cells to kill virus

171
Q

In an interferon alpha/beta primed cell, what does viral dsRNA do?

A

it activates RNAse L which degrades viral/host mRNA causing apoptosis

172
Q

interferon alpha/beta increases the expression of (Blank) molecules on nucleated cells/

A

MHC class I (molecules that present cytosolic proteins of cells to T cells to allow for the determination of whether the proteins are foreign or self i.e. they allow for self, nonself recognition)

173
Q

Where do NK cells come from?

A

from lymphoid progenitor cells

174
Q

How do you activate a NK cell?

A

with type I interferon and cytokines (tnf alpha and IL -12)

175
Q

What will NK cells produce?

A

large amounts of IFN-Y

176
Q

What do NK cells do?

A

kill virus infected cells, cells with intracellular pathogens and tumors by using cytotoxic granules to kill them

177
Q

What are the cytotoxic granules that NK cells use to kill stuff?

A

perforin and granzymes

178
Q

HOw do NK cells differentiate b/w self and non self?

A

through MHC class I molecule recognition and stress molecule

179
Q

NK cell deficiency can result in susceptibility to what viruses?

A

herpes

varicella (chicken pox and shingles), simplex 1 (oral) and 2 (genital) , epstein barr (mono) and cytomegalovirus

180
Q

What is antibody dependent cell-mediated cytotoxicity or ADCC?

A

when NK cells bind and kill antibody coated pathogens

181
Q

Wha t is the quickest response in a viral infection? what is the slowest/

A

production of interferon,TNF alph and IL2-> NK cell killing-> T cell killing

182
Q

What response lasts the longest in a viral infection?

A

T cell mediated killing

183
Q

The epithelial surfaces of the (blank), (blank) and (blank), which together with the skin, provide the first lines of defense against infection (chemical, mechanical, and physical barriers)

A

gastrointestinal, urogenital, and respiratory tracts

Block 6 Week 1 (13 decks)

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