Mediators Of Inflammation

Front 1

the cell which is a key link between the innate and adaptive immune systems

Back 1

dendritic cells

Front 2

zymogen

Back 2

inflammatory mediator that is present in plasma that needs to be activated

Front 3

how are zymogens usually activated

Back 3

proteolytic cleavage

Front 4

why do cytokines take longer to be released

Back 4

they are synthesized de novo

Front 5

Factor XII (Hageman factor) and complement are what two types of mediators (where are they found?)

Back 5

found in plasma - must be activated

Front 6

how do leukocytes get out of the blood vessel and into the interstitium

Back 6

diapedesis

Front 7

the initial step in diapedesis which involves transient adhesions is called? and emplys what kind of cell adhesion molecules

Back 7

"rolling" - involves selectins

Front 8

sticking and diapedesis involves what kind of cell adhesion molecules

Back 8

sticking: selectins and integrins
diapedesis: integrins

Front 9

histamine and serotonin are what kind of mediators

primary or secondar?

Back 9

pre-formed

Front 10

histimine is the principal mediator of

Back 10

immediate vascular permeability

(through H1 receptors)

Front 11

serotonin is released from platelet aggregation and causes

Back 11

increase vascular permeability

Front 12

how do ABs and C compare when it comes to heat lability

Back 12

Ab are heat stable and and Complement is heat liable

Complement is needed for Ab activation

Front 13

what complement is activated by Ag-Ab complexes

Back 13

classical pathway

Front 14

what pathway of C is activated by surfaces of pathogens

Back 14

alternative pathway -


note: complement is highly regulated

Front 15

two pieces of C that are important in inflammation

Back 15

C5a and C3a

Front 16

C that is important for phagocytosis

Back 16

C3b

Front 17

Complement that is important for lysis of microbe

Back 17

MAC

Front 18

the central component of complement is C3 which is converted to C3a and C3b by

Back 18

C3 convertatse

Front 19

C3b proteotypically cleaves

Back 19

C5

Front 20

MAC =

Back 20

C5b+ C6,7,8,9

Front 21

complement pieces that are known anaphyloxins

Back 21

C3a and C5a

Front 22

potent chemoattractant for and activator of PMNs (C)

Back 22

C5a

Front 23

Decay accelerating factor (DAF) has what effect on C system

(acts on what part of complement)

Back 23

deregulation of alternative pathway c3 convertase

it inhibits binding of factor B to cell associated C3B - causes intravascular hemolysis

Front 24

blocks MAC formation by blocking by blocking C7, C8 binding

Back 24

membrane inhibitor of reactive lysis MIRL

leads to deregulation of MAC and complement mediated intravascular hemolysis

Front 25

C1 inhibitor deregulates

Back 25

classical pathway -
causes HANE - hereditary angioneurotic edema

Front 26

what inhibits phospholipases which will ultimately inhibit all the formation of all products in the arachidonic acid cascade

Back 26

steroids

Front 27

COX inhibitors and aspirin inhibit the production of

Back 27

the production of prostaglandins

Front 28

prostaglanding that causes vasoconstricution, promotes platelet aggregation

Back 28

TXA2

Front 29

prostaglanding that causes vasodilation and inhibits platelet aggregation

Back 29

Prostacylin (PGI2)

Front 30

prostaglanding that causes vasodilation and potentiates edme

Back 30

PGE2

Front 31

Lipoxins cause what three things

Back 31

vasodilation
inhibit neutrophil chemotaxis
stimulate monocyte adhesion

Front 32

Leukotriene which is important for chemotaxis

Back 32

B4

Front 33

in general what is the effect of leukotrienes

Back 33

vasoconstriction
bronchospasm
increased permeability

Front 34

produced by the arachidonic cascade

local, short range hormones, formed rapidly, local effects, short lived

Back 34

eicosanoids

formed in specialized cellular domains called lipid bodies that have high concentraitons of synthetic enzymes

Front 35

eicosanoids that cause increase in vascular permeability

Back 35

LTC4, D4, E4

Front 36

eicosanoids that cause vasodilation

Back 36

PGI2,E2,E1, D2

Front 37

4 eicosanoids that cause vasoconstriction

Back 37

TXA2, LTC4, D4, E4

Front 38

eicosanoid that caused chemotaxis and leukocyte adhesion

Back 38

LTB4, HETE, lipoxins (inhibit)

Front 39

a chemokine w/ one a.a. separating first two conserved cys residues

Back 39

CXC (alpha)

Front 40

a chemokine with the first two cysteines are adjacent

Back 40

C-C (beta)

others
C = gamma
CxxxC

Front 41

what kind of receptor do chemokine bind

Back 41

7TM receptor - activating G proteins

Front 42

NO is released from

Back 42

endothelial cells

acts as a local paracrine factor, short lived,

Front 43

effect of NO

Back 43

vasodilation -

forms adducts with thiol groups on protein
Hemoglobin can function as NO sink - may be important function of hemoglobin

Front 44

two forms of NO that are constitutive at low levels and are ACTIVATED by Ca

Back 44

e-NOS, n-NOS

Front 45

iNOS is inducible and requires de novo synthesis w/in macrophages, does it require Ca

Back 45

no

Front 46

NF-kB induces the transcription of what cytokines

Back 46

TNF, IL-1

NF-kB is also stimulated BY these