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Sharks to be wary of in New Zealand waters. > Lecture 1 > Flashcards

Lecture 1 Flashcards

1
Q

Name the three major tracts covered by mucosal surfaces.

A 
Gastrointestinal (GI) tract- mouth down to anus.
Urogenital tract (genital and urinary organs)
Respiratory tract (upper and lower)
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2
Q

What defines mucosal surfaces?

A

Presence of epithelial cells secreting mucus.

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3
Q

What is the name of the human and microbiota together?

A

Supraorganism

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4
Q

What types of environmental impacts can affect microbiota configuration, leading to either eubiosis or dysbiosis?

A

Antibiotics
Other parasites/pathogens
Diet

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5
Q

How many cells are there within each part of the supra organism?

A

100 trillion microbiota cells

10 trillion our own cells

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6
Q

What 2 ways do microbes impact our bodies?

A

They release bad things such as toxins.

Or good things such as metabolites (SCFAs, vitamin K)

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7
Q

Give an example of how dysbiosis occurs through environmental pressure.

A

Antibiotics will reduce biodiversity, biomass and increase pathobionts such as C. difficile because it has less competition so it can thrive.

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8
Q

What makes up the microbiome?

A

Viruses, bacteria, microbial eukaryotes and fungi.

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9
Q

What are examples of pathogens interacting with each other?

A

Herpes simplex virus allows bacterial resistance
General virulence susceptibility due to bacterial presence.
Helminths cause autoimmune disease resistance
E. coli and entamoeba hystolitica increase virulence of eukaryotes.

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10
Q

What are the two functions of mucosal surfaces?

A

Exchange with outside, eg breathing., feeding/digestion, reproduction.
Forms barriers to chemical or biological insults

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11
Q

What helps to modulate the two functions of mucosal surfaces?

A

Epithelial cells and microbiota, the microbiota can affect exchange rates.

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12
Q

What are the primary mucosal defence systems?

A

Immediate innate defences:
Mechanical- tight junctions between epithelial cells.
Chemical- AMPS, lactoferrin, lysozymes, mucus.
Microbial- Microbiota producing h2o2, lactic acid, bacteriocins. Microbiota acting as mutualists competing for nutrients and attachment sites.

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13
Q

How do microbial defences work?

A

h2o2 provides protection from candida.

lactic acid protects us from viruses such as hiv.

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14
Q

What is the secondary defence?

A

Induced innate immunity- (after infection).

More AMPs, macrophages and Mucins.

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15
Q

What is the tertiary defence system?

A

Adaptive immunity- Immunoglobulins (SIgA) and cellular responses.

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16
Q

What do lysozymes target?

A

The walls of bacteria- peptidoglycan

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17
Q

What type of bacteria produce h2o2?

A

Lactobacillus is an example.

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18
Q

What are pathobionts?

A

members of the microbiota that have the potential to cause pathologies.

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19
Q

what is a treatment for C. diff that is antibiotic resistant?

A

Faecal transplant, its extremely effective, donor is usually a family member

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20
Q

what needs to be done before a fecal transplant?

A

donor must be screened for pathogens.

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21
Q

what effect does a healthy microbiota have on T cells?

A

it decreases the Th2 IgE response, and promotes Treg levels which is important to decrease inflammation at mucosal surfaces.

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22
Q

what are the 2 major types of epithelial tissues on mucosal surfaces?

A

Stratified epithelium- multiple layers of epithelial cells (present in the oral mucosa and vagina).
Simple epithelium- one layer of epithelial cells, present on digestive tract, respiratory tract and urogenital tract (urethra).

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23
Q

what is 16srRNA profiling?

A

a way of studying the composition of bacteria within the microbiome by using specific bacterial primers for 16s ribosome.

24
Q

what happens in mouse models if you completely remove the microbiota?

A

the immune system completely fails.

25
Q

what are the 5 ways that the microbiota confers health benefits to the host?

A

detoxification- changing toxins into harmless metabolites
biosynthesis- making vitamins, e.g vitamin k
immune maturation- induction of peyer’s patches, inducing mucosal T cells and IgA plasma cells.
metabolic- helps to digest dietary fibre.
protective- directly or indirectly.

26
Q

What do goblet cells and paneth cells produce?

A

goblet cells- Mucins

paneth cells- AMPs, lectins, cytokines

27
Q

What do goblet cells and paneth cells produce?

A

goblet cells- Mucins

paneth cells- AMPs, lectins, cytokines

28
Q

what is the length of the mucus layer?

A

10-700um

29
Q

describe the inner mucus layer

A

relatively sterile

rich in antimicrobial molecules

30
Q

describe the outer mucus layer

A

non-sterile, degrading mucus, microbes utilise mucin carbohydrates for energy.

31
Q

what are antimicrobial peptides?

A

peptides with selective microbicidal effects against bacteria, fungi and protists as well as viruses with a lipid envelope.

32
Q

how do AMPs kill pathogens?

A

they become anchored into the membrane and form pores which is lethal- also happens to the microbiota if it gets too close to the endothelium.

33
Q

what are mucus producing cells in the stomach called?

A

foveolar cells

34
Q

what is the structure of Mucins?

A

long proteins with repetitive elements with sugars attached to them.

35
Q

what are all epithelial cells derived from?

A

stem cells

36
Q

what are the four types of intestinal epithelial cells?

A

goblet cells, paneth cells, enteroendocrine cells and absorptive epithelial cells.

37
Q

what epithelial cell type can chron’s patients lose?

A

paneth cells

38
Q

what are the two compartments of the mucosal immune system?

A

the epithelium and lamina propria

39
Q

how are pathogens detected?

A

through pattern recognition receptors (PRRs) recognising pattern-associated molecular patterns (PAMPs).

40
Q

which cells express PRRs?

A

dendritic cells, macrophages and epithelial cells

41
Q

what are the 4 families of PRRs?

A

toll-like receptors (TLRs)
Nucleotide-binding oligomerisation domain-like receptors (NLR)
c-type lectin receptors (CLRs)
RIG-1 like receptors (RLR)

42
Q

what are c-type lectin receptors?

A

transmembrane proteins localised at the plasma membrane.

they recognise glycans from the walls of fungi and some types of bacteria

43
Q

what’s an example of a c-type lectin receptor?

A

dectin-1, which recognises B-1,3 glycans of the cell wall of various fungal species.

44
Q

what are NLRs?

A

cytoplasmic sensors with multiple subfamilies

45
Q

what are the 3 subfamilies of NLRs?

A

NLPRs- recognise bacterial, viral, parasitic and fungal PAMPs
AIM2- detects viral and bacterial DNA
NOD1 and NOD2- recognise bacterial peptidoglycan.

46
Q

what are toll-like receptors?

A

transmembrane proteins localised either at the plasma membrane or in endosomes.
they recognise proteins, nucleic acids, glycans

47
Q

what pathways do TLRs activate?

A

MAP kinase, NFkB and IRF

48
Q

what is an example of a tlr?

A

TLR4 recognises LPS, a component of the gram-negative cell wall.

49
Q

What are RIG-1 like receptors?

A

cytoplasmic sensors of viral RNA

trigger antiviral responses including the production of type 1 IFN

50
Q

what do RIG1 receptors signal via?

A

mitochondrial adaptor proteins (MAVs)

51
Q

What are examples of RLRs?

A

RIG-1 and MDA5

52
Q

How does the mucosal adaptive immune system response differ to its systemic counterpart?

A

It has specialised antigen sampling strategies
has distinct homing programme which allows immune effector cells to return to mucosal sites
specialised immune effectors including the secretary IgA (sIgA)
a variety of suppressive mechanisms

53
Q

why does the mucosal adaptive immune system response have a variety of suppressive mechanisms?

A

to maintain tolerance to environmental antigens (food)

to avoid inflammations against mucosal microbiota

54
Q

what are primary pathogens?

A

cause disease upon infection, usually not present in the host population

55
Q

what are opportunistic pathogens?

A

cause disease under circumstances, typically thrive in immuno-comprimised hosts, and can cause great damage.

Sharks to be wary of in New Zealand waters. (7 decks)

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