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Basic Immunology- Module 1 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is inflammation?

A

a complex response of vascularised tissues to infection and damage that brings cells and molecules frmo the circulation to the sites where they are needed–response of living tissue to injury

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2
Q

What cell type characterises acute inflammation?

A

neutrophils

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3
Q

What cell type characterises chronic inflammation?

A

macrophages

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4
Q

What is a granuloma?

A

a focal collection of inflammatory cells at sites of tissue infection especially activated macrophages (epithelioid cells)

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5
Q

What are the 4 common components of all inflammation?

A

inducers; sensor cells; mediators; target tissue

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6
Q

What is an inudcer

?

A

exogenous or endogenous signals that report tissues stress

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7
Q

What cells handle para-inflammation?

A

resident macrophages or mast cells

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8
Q

What is the tissue state in para-inflammation?

A

stressed or malfunctioning- not basal state but not damaged or infected

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9
Q

When does sterile inflammation occur?

A

in the absence of infection in response to cell damage or death

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10
Q

What can cause sterile inflammation?

A

trauma or ischaemic injuries- creation of DAMPs

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11
Q

Give examples of diseases that sterile inflammation has been implicated in?

A

gout; alzhemiers; atherosclerosis

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12
Q

What TLRs recognise HMGB1?

A

TLR2, 4 and 9

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13
Q

What receptor recognises cholesterol crystlas?

A

NLRP3 and CD36 (scavenger receptor)

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14
Q

What receptors recognsie beta-amyloid?

A

NLRP3; CD36 and RAGE

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15
Q

What receptor recognises uric acid and monosodium urate?

A

NLRP3

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16
Q

What is inflammaging?

A

upregulation of the inflammatory response that occurs with advancing age

17
Q

Why is there upregulation of inflammation with aging?

A

cumulative lifetime exposure of antigenic load or non infective antigens

18
Q

What happens to neutrophils in inflammaging?

A

reduced phagocytic ability of opsonised bacteria and impaired superoxide production

19
Q

What happens to monocytes/macrophages in inflammaging?

A

reduced MHC-II; reduced phagocytic ability and superoxide production

20
Q

What happens to DCs in inflammaging?

A

impaired ability to phagocytose apoptotic cells; impaired migration

21
Q

Waht happens to NK cells in inflammaging?

A

reduced cytotoxicity

22
Q

what happens to B cells in inflammaging?

A

reduced repsonsiveness to stimualtory molecules; antibody response to vaccination

23
Q

What is seen in the overall inflammation in inflammaging?

A

chronic low levels ofi nflammation concurrently with symptoms of immunosenescence

24
Q

What happens to T cells in inflammaging?

A

impaired expansion and differentiation; impaired T cell help to B cells; increased pro-inflammatory cytokine release; increased memory and effector cells; reduced Tregs

25
Q

How does the body counteract increased cytokines in the serum?

A

HPA axis is activated- cortisol levels increase

26
Q

Aside from the anti-inflammatory effects of cortisol, what other effects does activation of hte HPA axis cause?

A

protein catabolism; bone resorption; insulin resistance

27
Q

What can the higher levels of cortisol be counteracted with?

A

DHEA- although this also decreases with age

28
Q

What is autoinflammation?

A

self-directed inflammation, whereby local factors at sites predisposed to disease lead to activation of innate immune cells with resultatn tissues damage

29
Q

What is teh function of collagenous scavenger receptors?

A

phagocytosis of bacteria and apototic cells, endocytosis of modified LDL, adhesion

30
Q

Waht is the function of noncollagenous scavenger receptors (CD36)

A

phagocytosis of apoptotic cells; diacyl lipid recognition of bacteria

31
Q

Which TLRs recognise beta-defensins?

A

TLR1 and TLR2; TLR4

32
Q

How is can the diet interact with the immune system?

A

components of the diet e.g fatty acid can act as DAMPs for PRRs

33
Q

What effect does NFkB and MAPK signalling

A

reduce insulin signalling

Basic Immunology- Module 1 (31 decks)

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