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Block 6 Week 1 Colt > Innate Immunity - Hunter > Flashcards

Innate Immunity - Hunter Flashcards

1
Q

Describe colonization vs. infection:

A

Colonization is like having bacteria in your nose but not causing any problems; infection is when bacteria have broken your immune defenses and cause symptoms

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2
Q

Describe infection vs. disease:

A

Infection is when bacteria have made it into your body, while disease in when your cells have been damaged AS A RESULT of the infection.

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3
Q

What are opportunistic pathogens?

A

Pathogens that are on your body but only cause disease when you are immunosuppresed

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4
Q

What are the intrinsic epithelial barriers to infection?

A

Mechanical, chemical, and microbiological

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5
Q

Describe the mechanical intrinsic defenses of the skin?

A

epi cells joined by tight junctions

longitudinal flow of air or fluid

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6
Q

Describe the chemical defenses of the skin?

A
  1. fatty acids
  2. B-defensins (anti-microbial peptide)
  3. Lamellar bodies (seals the skin)
  4. cathelicidin (anti-microbial in lysosomes)
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7
Q

Describe the mechanical barriers of the gut?

A
  1. epi cells joined by tight junctions

2. longitudinal flow of liquid

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8
Q

Describe the chemical barriers of the gut?

A
  1. low pH
  2. enzymes (pepsin)
  3. alpha-defensins (cryptdins)
  4. RegIII (lecticidins)
  5. Cathelicidin
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9
Q

Describe the mechanical defenses of the lungs?

A
  1. epi tight junctions

2. Movement of mucus by cilia

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10
Q

Describe the chemical defenses of the lung?

A
  1. Pulmonary surfactant
  2. Alpha-defensins
  3. cathelicidin
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11
Q

Describe the mechanical defenses of the ENT cavities?

A
  1. epi tight junctions
  2. tears (physically wash away shit)
  3. nasal cilia
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12
Q

Describe the chemical defenses of the ENT cavities?

A
  1. enzymes in tears and saliva (lysozyme)
  2. Histatins (antimicrobial/antifungal)
  3. B-defensins
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13
Q

What are the three mechanisms of direct tissue damage by pathogens?

A
  1. Exotoxin
  2. Endotoxin
  3. direct cytopathic effects
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14
Q

Microbial pathogenesis involves (direct/indirect) damage of tissues

A

direct

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15
Q

Immunopathology involves (direct/indirect) damage to tissues

A

indirect

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16
Q

What are the three methods of tissue damage via immunopathology?

A
  1. Immune complexes
  2. Anti-host anitbody
  3. Cell-mediated immunity
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17
Q

What are the three antimicrobial ENZYMES?

A
  1. Lysozyme (tears)
  2. Pepsin (gut)
  3. Secretory phospholipase A2
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18
Q

How do defensins function?

A

Embeds itself in the bacterial membrane, dimerizes, and opens a pore

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19
Q

Defensins, cathelicidins, and histatins can all function because they have what kind of charge?

A

amphipathic

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20
Q

t/F: anti-microbial peptides are normally produced as pro-peptides

A

T

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21
Q

What cell type initiates inflammation once pathogens breach the epithelium?

A

macrophages

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22
Q

what two classes of chemicals do macrophages release to initiate the inflammation cascade?

A

chemokines and cytokines

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23
Q

(blanks) like TNF-a, cause vasodilation, increased vascular permeability, and upregulate expression of adhesion molecules to epithelium

A

cytokines

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24
Q

Chemokines attract what types of cells?

A

neutrophils (via CXCL8) and monocytes

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25
Q

Phagocytic cells, plasma cells, and the complement system engage and eliminate pathogens (before/during) the adaptive response is generated

A

BEFORE

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26
Q

Activation of what two systems during inflammation causes pain and blood clotting?

A

Kinin and coagulation

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27
Q

If the innate system works, is there a need for inflammation?

A

Nope

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28
Q

Macrophages recognize pathogens by (blank) encoded receptors

A

genome

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29
Q

What are the first two lines of defense if bacteria overrun tissue?

A

macrophages and complement system

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30
Q

T/F: neutrophils are more phagocytic than macrophages

A

true

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31
Q

What is on top of the PM in gram positive bacteria?

A

PDG layer with lipteichoic anchors and surface proteins

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32
Q

what is on top of the Pm in gram negative bacteria?

A

small PDG layer, then lipoprotein layer, then LPS layer

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33
Q

Do we want macrophages to recognize specific pathogens or patterns?

A

patterns

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34
Q

What are the four PAMPs for bacteria?

A
  1. f-Met-Leu-Phe receptor
  2. Mannose receptor
  3. Scavenger receptor
  4. LPS binding protein, TLR-4, and CD14
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35
Q

what are the two PAMPs for fungi?

A

Mannose recetpros and Dectin-1-glucan receptor. (if you leave sugary stuff out you will get mold)

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36
Q

What is the PAMP for viruses

A

Mannose

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37
Q

What is the scavenger receptor?

A

acetylated lipoproteins

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38
Q

LPS binding protein, TLR-4 and CD14 receptors are for gram (blank) bacteria

A

negative

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39
Q

How many human TLR genes are there?

A

10

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40
Q

TLR proteins are (blank) receptors

A

PAMP

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41
Q

T/F: TLR can be on the cell surface or endosomal

A

True

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42
Q

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

A

NF-Kb

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43
Q

Nucleoside Oligomerization Domain (NOD)-like proteins are similar to (blank) proteins

A

TLR

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44
Q

What do NODs do?

A

detect cytoplasmic bacteria and signal inflammation

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45
Q

What do retinoic acid inducible Gene (RIG) like proteins do?

A

detect viral RNA in the cytoplasm and signal inflammation

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46
Q

Are TLRs highly conserved?

A

yes

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47
Q

What is another name for LPS?

A

endotoxin

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48
Q

If pathogens invade the cytoplasm, (blanks) kick in and take over the job of TLRs

A

NODs

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49
Q

Where are RIGs located?

A

in the cytoplasm

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50
Q

What is the general cascade of PAMP producing danger signals?

A
  1. PAMP recognition
  2. TLR dimerization
  3. Intracellular signaling
  4. Gene expression
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51
Q

What protein is recruited by dimerized TLRs?

A

IRAK4 and IRAK1

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52
Q

How is NF-Kb produced?

A

IRAK4 mediated scaffolding releases TAK1 which leads to degradation of IkB and release of NF-Kb

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53
Q

IRAK-1 deficiency is a rare autosomal (blank) disease

A

recessive

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54
Q

How do you diagnose IRAK1 deficiency?

A

clinical suspicion and demonstation of poor response of monocytes to TLR agonists

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55
Q

What happens if you have no IRAK4?

A

No immune response via no inflammatory response via no cytokine release

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56
Q

A functioning inflammatory resposne is critical in host defense against (blank) bacterial infections, as evidenced in IRAK1 deficiency

A

pyogenic

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57
Q

What are the two major categories of defects in neutrophil function?

A

Defects in intracellular killing and adhesion defects

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58
Q

CGD, Chediak Higashi, and Type I integrin deficiency are all (blank)

A

defects in neutrophil function

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59
Q

CGD and G6PD deficiency are types of (blank)

A

abnormal respiratory burst

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60
Q

MPO deficiency, specific granule deficiency, and Chediak-Higashi are types of (blank)

A

granule abnormalities

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61
Q

Type I integrin deficiency and type 2 E-selectin ligand deficiency are types of (blank)

A

leukocyte adhesion deficiency

62
Q

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

A

Phagocytosis and intracellular killing

63
Q

What are the two methods in which particulate microbes are engulfed?

A

endocytosis and micropinocytosis

64
Q

What are the most important phagocytic cells?

A

macrophages and neutrophils

65
Q

Invagination of the cell membrane creates the (blank)

66
Q

Lysosomes filled with antimicrobial substance fuse with the phagosome to form the (blank)

A

phagolysosome

67
Q

T/F: most micbrobes are killed and digested in the phagolysosome

68
Q

what type of G-protein receptor is needed to form NADPH oxidase

A

GPCR C5a receptor

69
Q

where is NADPH in the phagolysosome?

A

membrane bound

70
Q

what does NADPH oxidase make that kills bacteria? What is this process called?

A

superoxide and hydrogen peroxide; the RESPIRATORY BURST–needs lots of oxygen to synth these molecules

71
Q

pH of the lysosome is lowered to…

A

activate hydrolases and antimicrobial peptides that kill the microbes

72
Q

What allows protons to be pumped into the phagolysosome to lower the pH?

A

NADPH oxidase

73
Q

what X-linked protein can cause NADPH oxidase defects if its is not present?

74
Q

What are the mechanisms of phagolysosome hostility?

A
  1. Acidification
  2. toxic oxygen species
  3. toxic nitrogen oxides
  4. antimicrobial peptides
  5. enzymes
  6. competitors
75
Q

What are the ROS?

A

superoxide, hydrogen peroxide, singlet oxygen, hydroxyl radicla, and hyphohalite OCl-

76
Q

What are the macrophage antimicrobial peptides?

A
  1. cathelicidin

2. elastase-derived peptide

77
Q

What are the neutrophil antimicrobial peptides?

A
  1. a-defensins (HNP1-4)
  2. b-defensins HBD4
  3. cathelicidin
  4. azurocidin
  5. bacterial permeability inducing protein (BPI)
  6. lactoferrin
78
Q

lysozyme digests the cell wall of some gram (blank) bacteria

79
Q

What are the phagolysosome competitors and what makes them?

A

neutrophils; make lactoferrin and B12 binding protein

80
Q

CGD is caused by the failure of (blank) in the phagolysosome

A

NADPH oxidase

81
Q

What causes the x-linked variant of CGD?

82
Q

What are the two modes of inheritance of CGD?

A

X-linked recessive and autosomal recessive

83
Q

Pyogenic bacteria and fungi cause (blank) on the skin and various organs in CGD

A

granulomatous lesions

84
Q

Flow cytometry using (blank) reveals a defect in the respiratory burst

A

dihydrorhodamine

85
Q

What is the treatment of CGD?

A

long term antibacterial and antifungal prophylaxis

86
Q

Is there a cure for CGD?

A

Tx with IFNg or bone marrow transplant

87
Q

What is the mode of inheritance of Chediak-Higashi?

A

autosomal recessive

88
Q

What is the molecular defect in Chediak-Higashi?

A

defect in microtubule polymerization; decreases phagolysosome formation

89
Q

When does C-H present and what how does it present?

A

Early childhood with recurrent pyogenic infections (staph and strep), especially GINGIVAL INFECTIONS

90
Q

Partial albinism is a sign of (blank)

A

Chediak-Higashi

91
Q

What is abnormal with neutrophils and eosinophils in C-H?

A

large lysosomal vesicles

92
Q

What is the Tx for C-H?

A

prophylactic antibiotics and bone marrow transplant

93
Q

Pt’s with (blank) also present with pyoderma

94
Q

what is the golden test for diagnosis of Chediak-Higashi?

A

peripheral blood smear, looking for humungous granules in neutrophils and eosinophils

95
Q

What is the most common defect in granulocyte-mediated defenses?

A

Neutropenia

96
Q

What are the causes of acquired neutropenia?

A

drug induced (especially chemo) and autoimmune (anit-neutrophil Abs)

97
Q

What are the three hereditary causes of neutropenia?

A
  1. Familial (benign, ethnic)
  2. Infantile genetic agranulocytosis (severe congenital neutropenia)
  3. Cyclic neutropenia
98
Q

Neutropenia leads to recurrent (blank) infections

99
Q

How do you measure neutropenia?

A

decreased absolute neutrophil count

100
Q

What is the lower limit for ANC?

A

1500-2000cells/mm3 blood

101
Q

Stapah, gram (blank) bacteria, fungi, and (blank) bacteria are common in neutropenia

A

gram negative and encapsulated

102
Q

Pyogenic bacteria and fungi can lead to life threatening neutropenic (blank)

103
Q

What is a common source of infection while in the hospital in pts with neutropenia?

A

in-dwelling catheter

104
Q

How do you treat neutropenic infections?

A

Broad spectrum antibiotics followed by targeted antibiotics once the bacteria is ID’d

105
Q

Pt’s with neutropenia are treated with (blank) before subsequent rounds of chemotherapy

A

human recombinant granulocyte colony stimulating factor (hrG-CSF)

106
Q

Severe Congenital Neutropenia (aka SCN or Kostmann Disease) presents at what age?

A

in infants

107
Q

How does SCN present?

A

recurrent infections of the skin, soft tissues, lungs, deep organs, and sepsis.

108
Q

What is the ANC level in SCN?

109
Q

SCN is caused by impaired (blank)

A

myelopoiesis

110
Q

Dx of SCN is supported by blockage of neutrophil differentiation at the (blank or blank) stage

A

promyelocyte or myelocyte stage

111
Q

rhG-CSF is used to treat patients with (blank), but risks myelodysplasia and acute myeloid leukemia

112
Q

Bone marrow transplants to treat SCN are only used when?

A

in infants refractory to rhG-CSF treatment

113
Q

neutrophils are called to sites of inflammation by tissue (blanks)

A

macrophages

114
Q

What are the four types of adhesion molecules?

A

VISI

  1. vascular addressin CD34
  2. Integrin (LFA-1)
  3. Selectin (L-selectin)
  4. ICAM-1
115
Q

CD18 is a component of which adhesion molecule?

116
Q

What are the four general steps of neutrophil migration?

A
  1. rolling adhesion
  2. tight binding
  3. diapedesis
  4. migration
117
Q

Is CD18 attached to the endothelium or to the neutrophil?

A

endothelium

118
Q

What molecule is used during rolling adhesion of neutrophils?

A

E-selectin

119
Q

What adhesion molecule is used during tight binding?

120
Q

Leukocyte Adhesion Def. type I presents with?

A

recurrent bacterial infections

121
Q

Adhesion molecule defects in LAD 1 result in (blank) ((3)

A

bad neutrophil chemotaxis, phagocytosis, and neutrophilia (increased Neuts)

122
Q

Omphalitis, pneumonia, gingivitis, and peritonitis are characteristic of (blank)

A

LAD type 1

123
Q

what is the inherited molecular defect in LAD type 1

A

deficiency of the B-2 integrin subunit of CD18

124
Q

How do you diagnose LAD type 1?

A

CD18 flow cytometry

125
Q

What is LAD type 1 Tx?

A

bone marrow transplant

126
Q

High levels of CRP indicate what?

A

an inflammatory process is active

127
Q

The acute phase response is mediated by (blank)

A

acute phase proteins, duh!

128
Q

CRP is a (blank)

129
Q

What binds and sequesters iron to stop bacterial growth?

130
Q

Fibrinogen is a (blank) factor

A

coagulation factor

131
Q

Fibrinogen levels correlate with (blank), an inflammation indicator

A

erythrocyte sedimentation rate (ESR)

132
Q

T/F: Albumin production is normal during acute phase

A

FALSE; albumin production is LOW

133
Q

Bacteria induce macrophages to produce IL6 which acts on (blank)

A

hepatocytes

134
Q

What are the acute phase proteins?

A
  1. serum amyloid protein
  2. CRP
  3. fibrinogen
  4. Mannose binding lectin
  5. SPA and SPD
135
Q

CRP binds (blank) on bacterial surfaces

A

phosphocholine

136
Q

CRP as as a (blank) activating complement when it binds to bacteria

137
Q

Mannose binding lectin binds to mannose on bacterial surfaces, acting as a (blank), activating complement

138
Q

Viral RNA induces interferon(blank) gene expression

A

alpha/beta

139
Q

Where does viral mRNA bind to signal for IFN expression?

A

endosomal TLR-3

MDA-5/RIG1/CARDIF in the cytosol

140
Q

What are the effects of IFNa and IFNb?

A
  1. induce resistance to viral replication in all cells
  2. increase expression of ligands for receptors on NK cells
  3. Activate NK cells to kill virus infected cells
141
Q

in an IFNa/b primed cell, viral dsRNA activates (blank), which degrades viral/host mRNA causing apoptosis

142
Q

IFNa/b increases the expression of (blank) on nucleated cells

143
Q

NK cells are derived from (blank)

A

lymphoid progenitor cells

144
Q

What activates NK cells?

A

Type I IFNs and cytokines (TNF-a and IL12)

145
Q

what cytokine do NK cells produce in large quantities?

146
Q

What two molecules do NK cells use to kill virus infected cells, cells with intracellular pathogens, and tumors?

A

perforins and granzymes

147
Q

Can NK cells recognize normal self MHC I?

148
Q

T/F: NK cells will kill cells that express stress molecules

149
Q

(blank) cell deficiencies will lead to severe/recurrent infections of herpes viruses (VZV, HSV, EBV, and CMV)

150
Q

What is the name of the process by which NK cells bind and kill antibody-coated pathogens?

A

antibody dependent cell mediated cytotoxicity

151
Q

Describe the timeline of innate immunity cytokine release and cell response?

A
  1. IFNa/b, TNF-a, and IL12 produced from 0-4 days
  2. NK mediated killing of cells from 0-6 days
  3. T-cell mediated killing of cells from 2 days onward
  4. Virus titer peaks around four days and lowers as T cell response grows

Block 6 Week 1 Colt (11 decks)

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