Inflammation Flashcards

1
Q

What causes heat and what are its benefits during infection?

A

The pyrogens Il-6 and IL-1B. They increase the metabolism of immune cells and decrease microbial growth.
PGE2 also acts on neurones to increase body temperature.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What causes redness and swelling? Benefits?

A

Extravasation from capillaries and post capillaires causes swelling, and increases leukoctye infiltration as well as infiltration of collections, pentraxins, complement, natural antibodies and ficolins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pain?

A

Caused by nociceptive stimuli, e.g. bradykinin and alarmins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How might inflammation contribute to loss of function?

A

increased infiltration of lymphocytes, smooth muscel contractin and over secretino of mucus. Inflammation break down of tight junctions (MCLK?0)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What 3 detrimental effects can inflammation lead to if not resolved?

A

Autoimmune disease and inflammatory tissue damage, sepsis.
Lack of tissue repair can cause fibrosis.
Adaption to stress- shift in homoestatic balance, Autoinflammatory disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What causes acute inflammatory responses? And what cells contribute?

A

Pathogens and tissue damage.
innate cells essentially, especially neutrophils NK cells, monocytes and other granuloctyes.
Maybe other innate like cells?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Primary mecahnisms of actue infections?

A

vasoactive amines and eicosanoids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why might eicosanoids take longer to react?

A

Synthesised through the arachindonic pathway.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Examples of eicosanoids?

A

PGE2 and leukotrienes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Functions of PGE2? And Luekotrienes?

A

Increase vasodilation and acts on neurones to act as a pyrogen. Very chemotactic for Th2 and eosinophils for the lungs.
Leukoctrienes also cause vasodilation and recruit neturophils.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does C3a and C5a contribute to acute inflammation?

A

C3a and C5a can bind to mast cells and stimulate histamine release- vasodilation and extravastion.
They can both also act as chemoattractant e.g, forneutrophils and macrophages.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

plsamin in actue inflammation?

A

breaks down fibrin clots, and cleaves complemet C3.

Also activates Factor XII.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What can factor XII do?

A

Factor XII can stimulate coagulation and fibrinolysis.

More importantly, factor XII activates the kinin system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what can bradykinin do?

A

pain, vasodilation and permeability and causes smooth muscle contraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Can PGE2 cause phenotypic changes to immune cells?

A

Yes, can act on DCs to increase their IL-23production, to favour Th17 cell differentiation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the two precursors and the products of the kinin system?

A

tissue kallikren and plasma kallikrin. Producees kalldin and bradykinin.

17
Q

Proteases in the kinin system

A

amino peptidases.

18
Q

Where is tissue and plasma kallikrein mostly found?

A

In the muscles and adipsoe.

Plasma kallikrein is in the liver mostly

19
Q

what two pathways are involved in the arachidonic system?

A

pathways that makes prostaglandin and the other lipoxygenase pathway that make leukotrienes and other anti inflammatory molecules.

20
Q

what enzymes are targeted by NSAIDs in the arachidonic pathway?

A

COX1 and COX2.

21
Q

What chemokines attract neutrophils? What receptors do neutrophils have?

A

CXCL1-7.

CXCR1 and CXCR2 important for neutrohpil migration.

22
Q

What chemokines attract lymphoctyes and monocytes? And what are the receptors for them?

A

CCL3,4 and 5.

Receptors are CCR5.

23
Q

What chemokines attrct B cells with receptors CXCR4 and CXCR5?

A

CXCL12 and CXCL13.

24
Q

What chemokines attract cell (T cells) with receptors CCR7?

A

CXCL19 and CXCL21.

25
Q

What is the ligand for CX3CR1?

A

CX3CL1.

26
Q

receptors in the IL-2 receptor family.

A

IL-2,4 IL-7,9 and Il-15 and Il-21. TSLP.

27
Q

What are HSP, ATP, uric acid have in commno?

A

They are all DAMPs.

28
Q

What components of the ECM can act as DAMPs? What TLR do they bind?

A

heparin sulfate, fibrinogen and tapasin C.

29
Q

What are two inhibitory compleemnt receptors?

A

CD55 and CD59.

30
Q

What does TLR9 recognise?

A

unmethylated CpG motfis on DNA.

31
Q

What can TLR5 bind?

A

TLR5 can bind flagellin.

32
Q

What does TLR 3 bind?

A

dsRNA

33
Q

What can TLR 7 and 8 detect?

A

ssRNA.

34
Q

What can TLR2 bind?

A

lipoproteins and glucans along with TLR6.

35
Q

What do NLRs like NALP signal through?

A

When bound to HSP90 in steady state has PyCARD domain that maintains pro capsapse 1.
K+ efflux in inflammation and procaspase 1 becomes activated and cleaves inactive forms of IL-1B and IL-18.

36
Q

What can NODs and NLPs and Rig like helciases sends?

A

bacterial peptidoglycans and RNA.

37
Q

What does NOD signal through?

A

RIP2

38
Q

how is NK-KB released?

A

IKKa and IKKB complex activated and phosphorylates IKB. IKB which was matinaing NF-KB is then degraded and NF-KB goes to nucleus.