Mediators of Inflammation Flashcards

(27 cards)

1
Q

What are the main mediators

A

Cytokines

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2
Q

Who mediates acute inflammation

A

TNF
IL-1
IL-17
Chemokines

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3
Q

Where does TNF come from

A

Macrophages, mast cells, T cells

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4
Q

What doe TNF do?

A

Expression of endothelial adhesion molc, release of other cytokines, systemic effects

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5
Q

Where does IL-1 come from

A

Macrophages, endothelial, some epithelial

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6
Q

Where do chemokines come from

A

macrophages, endothelial cells, T-cells, mast cells

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7
Q

Where does IL-17 come from

A

T-cells

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8
Q

Who mediates chronic inflammation

A

IL-12
IFN-gamma
IL-17

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9
Q

Where does IL-12 come from

A

dendritic cells, macrophages

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10
Q

Where does IFN gamma come from

A

T-cells, NK cells

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11
Q

What are arachidonic acid metabolites derived from

A

cell membranes, then cleaved by phospholipids

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12
Q

What is the name for the class of enzymes made from AA metabolites

A

eicosanoids

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13
Q

What are the types of eicosanoids

A

cyclooxygenase
lipoxygenase

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14
Q

What do cyclooxygenases produce

A

prostaglandins

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15
Q

What do lipooxygenases produce

A

leukotrienes and lipoxins

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16
Q

Why are AA metabolites so important

A

They produce and mediate almost every step of inflammation

17
Q

How are steroids and AAs related

A

Steroids act on phospholipases and prevent AA creation

18
Q

Pyrogens:

A

substances that induce fever

19
Q

How are fevers caused

A

IL-1 + TNF –> upregulate cyclooxygenases –> produce prostaglandins –> released into hypothalamus –> release neurotransmitters that increase body temp

20
Q

What are elevated acute-phase proteins

A

Plasma proteins synthesized in the liver

21
Q

What are the acute phase proteins

A

C-reactive protein
Fibrinogen
SAA

22
Q

What are some negative effects of inflammation

A

Septic shock
Secondary amyloidosis

23
Q

What causes septic shock

A

High levels of bacteria lead to large amounts of TNF and IL-1 being released
Eventually leads to DIC

24
Q

What causes secondary amyloidosis

A

Prolonged SAA production –> deposits of misfolded SAA
Can lead to tissue dysfunction

25
What does TNF do
Stimulates the release of other cytokines Stimulates endothelial adhesion molecules Upregulates cyclooxygenase Mediates granulocyte release Septic shock SAA production
26
What do lipoxins do
Inhibit neutrophil adhesion
27
What do leukotrienes do
Vasoconstriction Increase vascular permeability Leukocyte adhesion