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PHAR 510 > CHALK TALKS > Flashcards

CHALK TALKS Flashcards

1
Q

Night-like neutrophils:

A

no CXCR4 therefore released from BM

Increased proteins in granules
Decreased degranulation
Increased NETs

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2
Q

Day-like neutrophils:

A

no selectins therefore can’t reach tissue and remain in circulation

Increased granulation (bc occurs in cytoplasm)
Decreased NETs

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3
Q

Bmal1 deltaN mimics what type of neutrophil? survival?

A

Bmal1 deltaN mimics NIGHT-LIKE –> decreased survival

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4
Q

CXCR4 deltaN mimics what type of neutrophil? survival?

A

CXCR4 deltaN mimics DAY-LIKE –> increased survival

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5
Q

what controls granule content and amount of NETs?

A

Bmal1 and CXCL2/CXCR2 signaling

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6
Q

why must neutrophils be cleared and renewed?

A

to prevent vascular damage

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7
Q

what changes in neutrophils occur during aging and clearance?

A

changes in CD26L and CXCR4

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8
Q

how does CXCR4 affect BM-homing?

A

increased CXCR4 does not increase BM-homing

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9
Q

what are CD26L lo neutrophils phagocytosed by?

A

CD26L lo neutrophils phagocytosed by macrophages

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10
Q

what happens to neutrophil levels with a neutrophil transfer? why?

A

neutrophils increase bc of decreased G-CSF

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11
Q

are signals for HPC egress the same in steady state and inflammation?

A

no –> diff signaling for HPC egress depending on steady state or inflammation

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12
Q

how do macrophages support the hematopoietic niche?

A

producing protein factors

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13
Q

what does neutrophil engulfment trigger?

A

neutrophil engulfment triggers macrophages LXRs

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14
Q

neutrophil is sensor of _______

A

neutrophil is sensor of organism status

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15
Q

neutrophil clearance modulates ________

A

neutrophil clearance modulates non-BM macrophages

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16
Q

what are the main cells that catch bacteria in liver?

A

KCs

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17
Q

what does KC capture of bacteria depend on? what does it not depend on?

A

depends on CRIg but NOT opsonins

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18
Q

what type of bacteria can KCs capture?

A

UNOPSONIZED gram positive bacteria

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19
Q

what part of bacteria do KCs recognize?

A

LTA

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20
Q

what is essential for KCs capturing gram positive bacteria?

A

CRIg-LTA interaction

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21
Q

what type of mice did they use to find that KCs capture bacteria via CRIg?

A

used CR3 KO –> still able to capture bacteria (therefore complement system

used CRIg KO –> cannot capture bacteria, therefore CRIg is responsible

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22
Q

what is CR3?

A

dominant complement receptor for phagocytosis under static conditions on macrophages

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23
Q

at what stage of infection are AMs infected with Tb?

A

EARLY

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24
Q

what happens once AM are infected?

A

move from alveoli to interstitium

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25
what happens once AM are in interstitium?
recruits other immune cells to form granuloma and increases proliferation rate to further spread Tb
26
when do immune cells accumulate in interstitium?
BEFORE Tb spreads/before migration
27
what stimulates migration?
Tb activates INFLAMMASOME on non-HPCs via ESX secretion system which releases IL1 for MyD88/ILR1 signaling to allow AM to move to interstitium
28
what is BrdU?
incorporates into DNA of proliferating cells and can later be tracked and visualized with fluorescent Ab
29
what are CoH mice?
pet store mouse crossed with SPF mouse
30
CoH mice and UPEC
CoH mice have increased resistance against UPEC --> increased inflammation
31
CoH vs SPF spleens when infected with UPEC
both CoH and SPF spleens have increased neutrophils CoH have increased CD115+ monocytes
32
what is the result of CoH mice having increased CD115+ monocytes?
increased survival and clearance
33
what is mAb depletion?
Ab binds target on cell of interest and recruits immune killing of that cell
34
Ly6Chi vs Ly6Clo
Ly6Chi --> "ready state" + pro-inflammatory Ly6Clo --> "patroller state" + maintain homeostasis
35
are the CD115+ monocytes in CoH Ly6Chi or Ly6Clo? what is the significance?
Ly6Chi --> primed to respond quickly (INNATE TRAINED IMMUNITY)
36
In addition to Ly6Chi, what is found in high levels in CD115+ monocytes?
TNFalpha
37
what does BrdU of Ly6Chi CD115+ monocytes show?
increased migration of these monocytes from BM in CoH mice and increased myelopoeisis in CoH mice
38
what is the role of pyochelin?
made by PA via pqsA to inhibit S. aureus via iron chelation and ROS production
39
how does S. aureus defend against pyochelin?
methylates it
40
how was it found that S. aureus methylates pyochelin?
MALDI-MS and molecular networking
41
what methylates pyochelin?
Spm
42
how was it found that Spm is what methylates pyochelin?
library screening of S. aureus mutants and the complementation assay
43
how does methylation of pyochelin affect its function?
decreases ROS production and siderophore activity
44
how can you measure siderophore activity?
chrome azurol S assay CAS-Fe + Pch ----> CAS + Pch-Fe - CAS without Fe is fluorescent
45
3 things that occur in low-iron conditions
1. PA can grow without pyochelin 2. Pyochelin can REDUCE S. aureus growth 3. Met-Pch does NOT REDUCE S. aureus growth (bc lost ROS production and siderophore activity)
46
Pch in vivo
is Spm is mutated in vivo, S. aureus fitness does decrease but this does not affect the severity of the co-infection with PA
47
how does IAV affect pneumococcal disease?
IAV increases suceptibility to pneumococcal disease
48
what is the CRISPR system used to look at pneuomoccal infection?
doxycycline-inducible CRISPRi system
49
what does doxycycline do?
induces dCas9
50
why is the doxycycline-inducible CRISPRi system good? (2)
good for high-throughput quantitative genetic screening good for mapping infection bottlenecks in mouse model of pneumococcal pneumonia
51
do all mice deal with pneumococcal infection the same?
no, even genetically identical mice respond differently
52
which gene reduces pneumococcal virulence when targeted by the CRISPR system?
deletion of purA reduced in vivo fitness
53
which genes increase pneumococcal virulence when targeted by the CRISPRi system?
deletion of capsule genes promote bacterial viruelnce with IAV superinfection
54
what gene is NOT a good target for CRISPRi system? why?
MetK is poor target bc not essential in vivo
55
what allows the HepCCCleaver to enter the cell?
plasmid packaged in lipid shell allows entry via MEMBRANE FUSION-MEDIATED INTRACELLULAR TRANSPORT
56
what is membrane fusion independent of (2)?
1. endocytic process 2. lysosomal process
57
why is the membrane fusion-mediated intracellular transport good?
increases delivery efficiency and accessibility to nucleus
58
how do they make the HepCCCleaver specific to the liver?
use promoter that increases expression in liver cells
59
how can you sort cells to determine HepCCCleaver liver specificity?
sort cells with FACS
60
how do they make the HepCCCleaver specifically TARGET the liver?
galactose modification
61
how do they make the HepCCCleaver specifically target HBV viral proteins on the DNA?
guide the cleaver with gRNA to target conserved sites --> leads to decreased HBV proteins
62
how do they know that HepCCCleaver can accumulate in the liver?
detected increased Cas9 RNA in liver
63
longevity of HepCCCleaver anti-HBV therapeutic effects?
has continual anti-HBV therapeutic effects

PHAR 510 (11 decks)

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