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Microbiota On Mucosal > L1- Intro Mucosal Surfaces > Flashcards

L1- Intro Mucosal Surfaces Flashcards

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
Q

What do they do in gram -ve

A

Disrupt dna, rna and protein metabolism

Eg interfere with rna polymerase

26
Q

Give example

A

Thurin cd forming pores in C. difficile

27
Q

What are the top cells above crypt with brush border

A

Absorptive type

28
Q

Which other cells in intestine

A

M cells, enteroendocrine, paneth, m cells , tuft, goblet

29
Q

What forms after stem cells

A

Proliferatice progenitors then differentiated cells

30
Q

Which cell membrane bound mucin present in intestines and stomach

A

Muc1

31
Q

Where is glycocalyx and what is it

A

Above brush border
Mucins with other gp, gl and pgs

32
Q

What integrins do lp vs iel have

A

A4:b7 vs ae:b7 (mainly cd8)

33
Q

Why is mucin important for innate defences

A

They work best when dispersed in mucus eg iga and amps

34
Q

How can gastric muc6 have antimicrobial activity against hpylori

A

Blocks wall synthesis through its terminal

35
Q

How do cell surface differ in production

A

They are cleaved into 2 subunits in the er before trafficking to Golgi for glycosylation

36
Q

Why is this important

A

For shedding as some can act as binding sites eg Lewis b ag on muc1 for hpylori babA

37
Q

Which other way can microbes induce exocytosis of goblet cell mucin

A

Nlrp6 activation eg via tlr - myd88- ros gen- nlrp6

Eg listeriolysin-o

38
Q

Does mucosal immunity in gut get input systemic immunity

A

No it is all mucosal unlike others like lungs

39
Q

What time frame is induced innate and induced adaptive killing

A

Innate is 4-96hours

40
Q

Give 2 examples of exotoxins by pathogens

A

TcdA /b by cholera

Shifatoxin from e:0137

41
Q

Immune complexes are indirect pathogenic effects of pathogens. Give example

A

Yellow fever
Ebola

42
Q

How can they be pathogenic

A

Eg hanta virus glomerulonephritis

43
Q

Give example of anti-host antibodies pathogenicity

A

Strep pyogenes antibodies can cause rheumatic fever via attacking heart tissue

44
Q

Which immune responses needed for intracellular cytoplasmic cvs vesiclular

A

NK and cd8
Also activated macrophages (ifny?)

45
Q

What are effector modules

A

3 types of responses against particular type of pathogen using particular cell and humoral responses

46
Q

What is module 1 for

A

Intracellular cytotoxicity and elimination of infected/stressed cells

Th1, ilc1, NK

47
Q

What is module 2 for

A

Mucosal and barrier immunity eg for parasites (th2, ilc2)

48
Q

What is module 3 for

A

EC immunity

fungi, protists, bacteria etc

Th17, ilc3 response , recruiting neutrophils

49
Q

Pathogenic induced release of what cytokines induce NK and ilc1 stimulation

A

Il12/il18 (both th1)

50
Q

What does this in return cause

A

Granzyme and perforin killing

Ifny release by both

Macrophage activation

51
Q

What cytokines induce ilc2

A

Il25,33,tslp

52
Q

What do they release in turn and what for

A

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
Q

What is module 3 stimulated by

A

Il1b, il23

54
Q

What do ilc3 then release and what for

A

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
Q

What do Ilc help do

A

Intermediatelt connect innate with adaptive

Also give appropriate response to microbes

56
Q

Where do they all predominate although all 3 in all sites

A

Skin ilc1

Lung ilc2

Gut ilc3

57
Q

Which ecoli probiotic strain is able to absorb all iron to compete with salmonella via siderophore (largest iron acquisition genes)

A

Ecoli nissle 1917

58
Q

Which sort of adhesion molecules does it have whcih blocks pathogens and is why it’s given for Ibd treatment

A

Curli ligand

59
Q

Which commensal species have T6SS important also for toxin delivery

A

Bacteroides

60
Q

How does lactobacillus Reuteri induce il22 by ilc and why is this important for barrier

A

Trp metabolism to indole3 aldehyde which stimulates the Aryl hydrocarbon receptor on ilc to release i22

Needed for tj formation, mucus and amps

61
Q

How is il10 anti inflammatory

A

Downregulated of cytokine exp and also MHC II presentation
Aswell as inducing treg differentiation

62
Q

How do il4 and il13 stimulat mucin expression from goblet cells

A

Through inducing spdef tf

Microbiota On Mucosal (22 decks)

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