L1- Intro Mucosal Surfaces Flashcards

(62 cards)

1
Q

What is the sa of mucosal surfaces

A

120m2
75 resp
40 gi

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2
Q

What sorts of cells like the gi tract from stomach vs lungs

A

Simple columnar

Lungs is simple squamous

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3
Q

What’s the diff between immediate innate and induced innate

A

Immediate is already present eg mucins, Amps, tj, Microbiota colonisation resistance

Induced is with the help of immune cells like neutrophils

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4
Q

Which amps are present in gut

A

A defensins, reg3 lecticidins, cathelicidins

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5
Q

Is the lung the same

A

Yes except no reg3

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6
Q

What mechanical methods is there

A

Ciliary mucosal system

Tight junctions

Low ph in stomach

Continuous shedding of cells (exclusion)
Coughing and peristalsis

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7
Q

Which pro-cytokines released by mac indirectly by Microbiota causes neutrophil attraction

A

Il1b

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8
Q

What direct competition is there using Microbiota

A

Limited carbon sources
Bacteriocins , lactic acid, h202
Compete with adhesion

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9
Q

Which cells are some you haven’t heard of before and what do they do

A

Tuft cells
They sense parasites/microbes and induce a type 2 response and goblet cells activation

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10
Q

What do paneth release

A

Cytokines, lectins, Amps

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11
Q

What tlr9 ligand stimulates paneth dengranularion via the myd88 pathway

A

Cpg unmethylated ef from virus or bacteria/microbiota

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12
Q

What do lysozymes hydrolyse and why do they work best for gram +be

A

The b-glycosidic links in peptidoglycans

Gram +ve have exposed peptidoglycan cell wall not covered by om

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13
Q

Which microbes do a/b defensins, cathelicidins and lecticidins(reg3) work on

A

Fungi, bacteria, Protozoa, enveloped viruses

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14
Q

Why can they interact with the phospholipids through electrostatic interaction

A

They are all positive compared to negative phosphate heads

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15
Q

Which defensins is major in the gi tract

A

A defensin

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16
Q

What are the 2 major forms of a defensin

A

Hd5 and 6

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17
Q

What do they form in the phospholipid membrane

A

A dimer causing a pore

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18
Q

Which enzymes needed to convert pro-adefensin to a defensin

A

Trypsin

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19
Q

How is hd6 diff

A

Not bacteriocidal it traps them in a net above mucus

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20
Q

What other amp needs trypsin

A

Reg3a

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21
Q

What shape does reg3 form in phospholipids

A

Heaxemric (3dimers)

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22
Q

How does pore kill bacteria

A

Permeates it to ions, which kills bacteria through depolarisation

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23
Q

How is ll37 cathelicidins different

A

They form an a helical structure when in contact with membrane through electrostatic interaction and then insert in to form pore

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24
Q

Bacteriocins are similar to amps. What do they do in gram +ve

A

Form pores / disrupt cell wall/membrane

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25
What do they do in gram -ve
Disrupt dna, rna and protein metabolism Eg interfere with rna polymerase
26
Give example
Thurin cd forming pores in C. difficile
27
What are the top cells above crypt with brush border
Absorptive type
28
Which other cells in intestine
M cells, enteroendocrine, paneth, m cells , tuft, goblet
29
What forms after stem cells
Proliferatice progenitors then differentiated cells
30
Which cell membrane bound mucin present in intestines and stomach
Muc1
31
Where is glycocalyx and what is it
Above brush border Mucins with other gp, gl and pgs
32
What integrins do lp vs iel have
A4:b7 vs ae:b7 (mainly cd8)
33
Why is mucin important for innate defences
They work best when dispersed in mucus eg iga and amps
34
How can gastric muc6 have antimicrobial activity against hpylori
Blocks wall synthesis through its terminal
35
How do cell surface differ in production
They are cleaved into 2 subunits in the er before trafficking to Golgi for glycosylation
36
Why is this important
For shedding as some can act as binding sites eg Lewis b ag on muc1 for hpylori babA
37
Which other way can microbes induce exocytosis of goblet cell mucin
Nlrp6 activation eg via tlr - myd88- ros gen- nlrp6 Eg listeriolysin-o
38
Does mucosal immunity in gut get input systemic immunity
No it is all mucosal unlike others like lungs
39
What time frame is induced innate and induced adaptive killing
Innate is 4-96hours
40
Give 2 examples of exotoxins by pathogens
TcdA /b by cholera Shifatoxin from e:0137
41
Immune complexes are indirect pathogenic effects of pathogens. Give example
Yellow fever Ebola
42
How can they be pathogenic
Eg hanta virus glomerulonephritis
43
Give example of anti-host antibodies pathogenicity
Strep pyogenes antibodies can cause rheumatic fever via attacking heart tissue
44
Which immune responses needed for intracellular cytoplasmic cvs vesiclular
NK and cd8 Also activated macrophages (ifny?)
45
What are effector modules
3 types of responses against particular type of pathogen using particular cell and humoral responses
46
What is module 1 for
Intracellular cytotoxicity and elimination of infected/stressed cells Th1, ilc1, NK
47
What is module 2 for
Mucosal and barrier immunity eg for parasites (th2, ilc2)
48
What is module 3 for
EC immunity fungi, protists, bacteria etc Th17, ilc3 response , recruiting neutrophils
49
Pathogenic induced release of what cytokines induce NK and ilc1 stimulation
Il12/il18 (both th1)
50
What does this in return cause
Granzyme and perforin killing Ifny release by both Macrophage activation
51
What cytokines induce ilc2
Il25,33,tslp
52
What do they release in turn and what for
Il4, il13, il5 (th2 cytokines) Amphireglin - binds egfr for tissue remodelling = barrier Allows mucus production (by il13 and il4 spdef tf) ecm remodelling/tissue repair (by m2 shift which releases tgfb)
53
What is module 3 stimulated by
Il1b, il23
54
What do ilc3 then release and what for
Il17, 22 , gmcsf For antibody (il17) , 22 for amp release, maturation of apc/phagocytosis Gmcsf is however also anti inflam via inducing ra and il10 release
55
What do Ilc help do
Intermediatelt connect innate with adaptive Also give appropriate response to microbes
56
Where do they all predominate although all 3 in all sites
Skin ilc1 Lung ilc2 Gut ilc3
57
Which ecoli probiotic strain is able to absorb all iron to compete with salmonella via siderophore (largest iron acquisition genes)
Ecoli nissle 1917
58
Which sort of adhesion molecules does it have whcih blocks pathogens and is why it’s given for Ibd treatment
Curli ligand
59
Which commensal species have T6SS important also for toxin delivery
Bacteroides
60
How does lactobacillus Reuteri induce il22 by ilc and why is this important for barrier
Trp metabolism to indole3 aldehyde which stimulates the Aryl hydrocarbon receptor on ilc to release i22 Needed for tj formation, mucus and amps
61
How is il10 anti inflammatory
Downregulated of cytokine exp and also MHC II presentation Aswell as inducing treg differentiation
62
How do il4 and il13 stimulat mucin expression from goblet cells
Through inducing spdef tf