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Infection and immunity > 16. Host Pattern Recognition and Avoidance > Flashcards

16. Host Pattern Recognition and Avoidance Flashcards

1
Q

Why could allergy and autoimmune conditions be increasing?

A

hypothesis: a lack of exposure to pathogenic and commensal bacteria caused by a more clean modern environment

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2
Q

what is transient exposure?

A

specific short term exposure experienced by people at different points in time

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3
Q

What is the most common type of exposure to pathogens?

A

transient

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4
Q

why is commensal flora essential for life?

A

they help the body sense bacteria and respond appropriately to both commensal and pathogenic bacteria

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5
Q

why is the absence of TLR stimulation detrimental to health?

A

causes dysregulation of signalling pathways causing a lack of response to tissue damage and lack of barrier integrity

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6
Q

What helps develop the signalling pathways?

A

the commensal microbiota stimulating signalling pathways

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7
Q

what is an immunological paradox?

A

the cells interacting with the microbiota need to decide what to tolerate and what to mount an immune response to

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8
Q

What is needed to maintain barrier function?

A

Stimulation of TLR and NLR by commensals helps maintain intestinal homeostasis

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9
Q

what is the normal immune response signalling pathway?

A

Recognition of PAMPs by PRR
signal transduction
induce changes in gene expression
(inflammation)

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10
Q

what is one of the most commonly studied TLR?

A

TLR-4 that recognises LPS

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11
Q

why is compartmentalisation of TLR receptors important?

A

So the receptors are in the right place to detect the pathogen motif and the response occurs in the correct place in the cell

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12
Q

where would TLRs that detect lipoproteins LPS and viral components be?

A

on the external surface of the cell

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13
Q

Where would TLRs that detect pathogenic RNA/DNA be?

A

on the endosome

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14
Q

What are the roles of TLRs and NLRs?

A

regulate NF-kB, MAPK, IRF pathways that cause proinflammatory and antimicrobial gene products

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15
Q

what effects do TLR have on immature dendritic cells?

A

Activate them
secrete cytokines
express costimulatory molecules
express MHC-2
Induction of migration to secondary lymphoid organs

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16
Q

What is the distribution of PRRs in mammals?

A

not all cells express all PRR
different TLR, NLR and RIH are expressed differently in different cell types and different cell compartments

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17
Q

what do all PRRs do?

A

signalling cascades that regulate gene expression to counteract infection
proinflammation
antimicrobial peptides

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18
Q

What should PAMPS really be called?

A

MAMPS - microbe-associated molecular patterns

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19
Q

can the microbiota trigger PRR?

A

yes they all have pathogenic components

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20
Q

why doesn’t the microbiota trigger an immune response?

A

to distinguish between commensal and pathogenic bacteria a secondary signal must be needed to trigger the response

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21
Q

What is the Janeway hypothesis?

A

that a second signal is needed to trigger a full immune response to ensure the response to proportional to the pathogen

22
Q

what is the first signal needed for a full immune response?

A

PAMP - PRR interaction to prime the immune system

23
Q

what is the second signal needed for a full immune response?

A

Patterns of pathogenesis

24
Q

what are patterns of pathogenesis?

A

cell or tissue damage
molecules secreted by infected cells
detection of secreted toxins

25
when do you gain you gut microbiota?
As soon as amniotic sack bursts you start to be colonised
26
what are the first bacteria to colonise the gut?
Enterobacteria, Bifidobacteria then firmicutes and bacteriodetes
27
why is it important to acquire the right sort of organisms?
dangerous if you acquire the wrong sort of bacteria too early the right bacteria will create an environment suitable for them and prevent the growth of other pathogenic bacteria
28
what are the main ways you acquire microbiota?
ingestion and inhalation
29
Why do we understand very little about the microbiota?
most organisms cannot be cultured in the lab to be studied and sequenced need integrated studies
30
what happens to the diversity of bacteria as you go down the GI tract?
it increases with the colon being the most diverse
31
how many bacteria are in the colon per human cell?
1.4 bacterial cells to 1 human cell
32
what are the protective functions of the gut microbiota?
exclude pathogens compete for nutrients, receptors and between themselves use up adverse nutrients for us
33
what are the structural functions of the gut microbiota?
Stimulate TLR to fortify gut barrier Tightening cell junctions to prevent leaky intestines stimulate IgA production immune development
34
what are the metabolic functions of the gut microbiota?
GOOD: use up carcinogens making vitamins and vitamins precursors fermenting what we can't so we can use the product eg complex carbohydrates BAD: metabolising drugs preventing treatments being fully effective
35
What broader impacts can the microbiota have?
behaviour anxiety blood vessel formation tissue homeostasis eating habits
36
how many of our immune cells are associated with the gut?
30-40%
37
what are the 5 major cell type in immune sensing in the gut?
intestinal epithelial cells M cells Macrophages Dendritic cells Intra epithelial lymphocytes
38
what happens in normal immune homeostasis?
commensal bacteria stimulate PRRs and tighten tight junctions
39
what happens when a pathogen enters normal immune homoestasis?
dysregulation of TLR signalling over response loosening of junctions bacteria cross the epithelial barrier bacteria enter substital fluids and blood
40
what innate precautions do we have to prevent inappropriate immune activation?
More PRRs in deeper tissues as commensal are only at the apical surface the commensal have low affinity for PRR as they don't have adhesins trapping of commensal by surface mucus
41
what PRR are in the intestinal crypt?
TLR2, TLR4, NOD1, NOD2
42
what do pathogens have that commensals don't?
mucinases Adhesins Invasins type 3/4 secretion system haemolysins exposure of TLR Engagement of NLR
43
what keeps commensal from activating the immune system?
lack of virulence factors less agonistic PAMPs weak TLR activity Life in biofilms on the mucus surface controlled diffusion of PAMPs
44
why do we think pathogens evolved from commensals?
to overcome host defences the immune system selects the pathogen with the ability to overcome its function
45
how can the bacterial pathogens overcome host defences?
modulate innate immunity modulate adaptive immunity by diminishing recognition and memory stealth to evade early immunity secreted virulence factors subvert immune response by causing Cell and tissue lesions
46
how do pathogens modulate immune response?
avoid PRR avoid death by Polymorphonuclear leukocytes prevent pro-inflammatory signalling inactivating immune cells binding to inhibitory motifs
47
How does changing the acylation of lipid A avoid the immune system?
having 6 acyl chains will activate PRR having 5 acyl chains has a much lower affinity for the PRR all done through phase variation depending on temperature
48
how can type 3 secretion systems subvert immune responses?
injecting effector proteins YOP proteins Lethal factor
49
how can toxins prevent MAP kinase and NF-kB pathways activation by TLR?
suppress secretion of effector proteins avoid immune detection by preventing signalling molecules many different points of the pathway can be suppressed
50
what is the MAP kinase pathway?
Mitogen activated protein kinase pathway
51
what is the key point about the commensals and pathogen dynamic?
there are constant interactions and the decisions of tolerance of important
52

Infection and immunity (22 decks)

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