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Immunology week 6 > Mucousal immunity I > Flashcards

Mucousal immunity I Flashcards

1
Q

What are the three modes of innate defense in mucosal immunity?

A

mucus produciton, AMPs and IgA

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2
Q

What levels of immunity are there in mucosal surfaces?

A

pre epithelial (mucus and IgA), epithelial (AMPs and tight junctions) and sub-epithelial (innate and adaptive immune cells).

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3
Q

What specialised cells are there in gastric pits?

A

perietal cells (produce HCL), chief cells (produce pepsinogens and lipases), G cell (gastrin) and specialised mucus producing cells (goblet cells?)

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4
Q

What is mucus made up of?

A

water + mucins (glycoproteins and lipids)

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5
Q

How are epithelial cells protected form pathogens and low pH of stomach?

A

tight juncitons, mucus, and secretino of bicarbonate which in mucus creates a pH gradient.

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6
Q

What kind of infectino can cause ulcers?

A

H. pylori infeciton

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7
Q

How does H pylori cause ulcers?

A

They produce urease, which will breakdwon urea into ammonia.
Ammonia protects them from pH, but is toxic to epithelial cells that then become exposed to low pH.

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8
Q

Test for H. pylori infeciton?

A

C13/C14 tablet and breath test as urea broken down into ammonia and CO2.

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9
Q

What beneficial functions does mucus offer?

A

lubricant, stable microenvironment that is essential for microflora. Prevents invasion of pahogens.

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10
Q

How is mucus stratified

A

Has a dense layyer with small pores (prevents bacterial penetration). Above is a loose layer where porteases have broken down glycoprotiens to form larger pores where bacteria are.

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11
Q

why is mucus important for microflora and what happens when it breaks down.

A

Helps to separate microflora from the epithelium.

Breakdown, bacteria come into contact with epithelium.

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12
Q

Why have different kinds of mucins?

A

Glycan repertoire can slect for diffeent microorganisms.

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13
Q

When might upregulation of mucus e.g. muc5ac be beneficial?

A

During infection (especially of nematode infecctinos). Mucus removal is greater than that of epithelial cells.

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14
Q

What immune factors can stimulate goblet cells

A

histamine, acetylcholine and pGE2.

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15
Q

how might microflora be beneficiala nd help prevent infection?

A

Can provide metabolites and vitamins.

Provides a barrier and can out compete other potential pathogens.

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16
Q

What virulence genes can commensal E.coli acquire? What are its effects?

A

Shiga toxin,

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17
Q

what are effects of E.coli producign shiga toxin?

A

makes it pathogenic allows invasion and enhances mucus production with traps bacteria and creates a biofilm to cause diarrhea.

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18
Q

diseases associted with mucus overproducion?

A

CF, traps bacteria within the respiratory tract leads to severe infection.
Asthma.

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19
Q

What site are commensal bacteria S. aureus and Corynebacterium associated with?

A

nasal and oral cavity.

20
Q

Does respiratory tract have microbiome?

A

yes

21
Q

What cells in crypt produce AMPs? And where about are they localised?

A

Panneth cells produce AMPs at bottom of the crypt.

22
Q

What immune related signalling pathway can activate panneth cell AMP secretion?

A

TLR MyD88 dependent signalling. Can upregulate defensin and RegIII gamma production.

23
Q

What can RegIII gamma production do?

A

keeps bacteria away from epithelium- influences microflora.

24
Q

Another two defensins?

A

human defensin 5 and 6.

25
Q

What patinets are goblet HD5+ cells seen in? What might this say?

A

in ulcerative colitis patients. May suggest that microbiome dysbiosis can influence the immune AMP response.

26
Q

Is there a perfect microflora?

A

No individual or standard healthy microflora. But there are genetic variants whihc are associated with microbiome dysbiosis.

27
Q

Microbiome targeted treatment of Ulcerative colitis?

A

probiotics and faecal transplants from healthy donor.

28
Q

Risk of faecal transplant?

A

Risk of c. difficiel infection, whihc has high mortaliity.

29
Q

What effects can c. difficile toxin have?

A

breakdown tight junctions, cause direct cytoxicitty of epithelium and induce inflammation.
Can cause pseudomembranatous colitis.

30
Q

What increases risk of C. difficile infection?

A

lower microbial diversity, e.g. due to antibiotics.

31
Q

What treatment can restore c. difficle infection?

A

faecal transplant!

32
Q

How is IgA secreted?

A

Binds to polymeric Ig receptor (pIgR) which forms a complex that is endocytosed and transported across epithelium and into the lumen.

33
Q

How is IgA persist in the mucous/lumen

A

the secretory component of the pIgR prevents sIgA proteolysis.

34
Q

3 modes of IgA protection?

A
  1. Neturolisation of infection/attachement
  2. binds and mediates enodcytosis and intracellular killing of pathogen.
  3. can bind antigen in lamina propria, and excrete it into lumen via secretory pathway.
35
Q

How is IgA secretion upregulated in response to infection?

A

Because inflammaation induces pIgR upregulation.

36
Q

what other situations apart from infection can IgA be protective.

A

May have anti- allergy effects.

37
Q

3 evasion mechanisms of neisseria infections?

A
  1. secretes a IgA protease.
  2. sialylates its LPS to avoid complement activation.
  3. blebbing of membrane adsobrs and depletes IgA.
38
Q

Where can IgA plasma cells be produced?

A

peyers patcehs, lamina propia, cyptopatches.

39
Q

Is IgA production T cell independent or dependent?

A

Can be both.

40
Q

What cells does T cell independent IgA actiatino need?

A

Need ILCs and pDCs for IgA class switching.

41
Q

What is odd about IgA in patients with colitis?

A

Iga highly coats colitogenic bacteria- not neutralising.

42
Q

Gaps between panneth cells are where cryp base columnar stem cells are. They adhere to panneth cells, how might panneth cells offere protection for this niche?

A

by producing AMPs for a sterile area. Ensures that stem cells are replenished.

43
Q

What happens if you don’t get enough renewal or increased death of epitherilium?

A

Increased detah leads to loss of barrier function and loss of AMP production allowing commensal invasion.

44
Q

What happens if you get overproliferation of the crypt?

What pathogen causes this and what disease does it look like?

A

You lose differentiation, proliferative zone expans and surface area decreased and functional performance impaired.

Girardia intestinalis and Looks a bit like coelia disease.

45
Q

If you see greater proliferatino and lareger crypts, what infection might this benefit?

A

may benefit helminth infections, as they burrow through the top of epithelium to make their niche.

Immunology week 6 (7 decks)

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