mediators of local/systemic inflammation- week 2 Flashcards
what are cytokines
proteins produced by many types of cells that mediate immune and inflammatory reactions
what cytokines are in acute inflammation
TNF, IL-1, Chemokines, IL-17
What cytokines are in chronic inflammation
IL-12, IFN-gamma, IL-17
what are principle sources of TNF
macrophages, mast cells, T cells
what are principle sources of IL-1
macrophages, endothelial cells, some epithelial cells
what are principle sources of chemokines
macrophages, endothelial cells, T cells, mast cells
what are principle sources of IL-17
T cells
what is the action of TNF
stimulated expression of endothelial adhesion molecules, release of other chemokines, has systemic effects
what are principle actions of IL-1
similar to TNF
what are principle actions of chemokines
leukocyte recruitment
what are principle actions of IL-17
neutrophil, and monocyte recruitment
what are cytokines of chronic inflammation
IL-12, IFN-gamma, IL-17
what are principle sources of IL-12
dendritic cells, macrophages
what are principle sources of IFN-gamma
T cells, NK cells
what are principle sources of IL-17
T cells
what are principle actions of IL-12
increased production of IFN-gamma
what are principle actions of IFN-gamma
increased ability of macrophages to kill microbes and tumor cells
what are principle actions of IL-17
neutrophil and monocyte recruitment
other ________ of inflammation work in concert with cytokines
mediators
arachidonic acid is derived from_______
cell membranes
___________ or release of other mediators causes release of AA from cell membrane
injury/irritation
active AA is released via _________
cleavage by phospholipases
AA is further metabolized to create 2 classes of enzymes
cyclooxygenase
lipoxygenase
what does cyclooxygenase generate
prostaglandin
what does lipoxygenase produce
leukotrienes and lipoxins
drugs that inhibit enzymes that are responsible for creating AA metabolites are used to treat________
inflammation
_______ act on phospholipases
steroids
AA metabolites have what response
vascular reactions, leukocyte chemotaxis
(vasodilation/vasoconstriction/leukocyte adhesion, inhibition of neutrophil adhesion, CHEMOTAXIS)
systemic effects aka
acute phase response
examples of systemic effects
fever
elevated levels of acute phase proteins
leukocytosis
which molecules are involved in systemic inflammation effects?
AA metabolites: leukotrienes, prostaglandins
Cytokines (IL-6, IL-12, TNF)
Cytokines (IL-1, IL-6, TNF) mediate _______
leukocyte recruitment and migration
substances that induce fever:
exogenous substances (LPS)
endogenous substances (IL-1, TNF)
exogenous substances that cause fever cause cells to release _______
endogenous substances (IL-1, TNF)
IL-1 and TNF upregulate
cyclooxygenases
cyclooxygenases synthesize
prostaglandin
prostaglandins are released by ______ and stimulate the release of neurotransmitters that reset the body’s temp to a higher level
hypothalamus
in fever, temp reset is via _________ and by increasing heat production via _________
vasoconstriction (reduce heat loss)
effect on brown fat and skeletal muscle
most plasma proteins are synthesized in the
liver
examples of plasma proteins
C reactive protein
fibroinogen
serum amyloid A
CRP is simulated by
IL-6
fibrinogen is stimulated by
IL-6
SAA is stimulated by
IL-1 or TNF
SAA and CRP may act as opsonins by
binding to bacterial walls or interact with complement
-may bind chromatin (helps clear necrotic cells)
-CRP levels measured to detect inflammation
fibrinogen binds to RBC and causes them to form ______ which causes blood to _________
stacks
sediment faster
leukocytosis initially occurs because of
increased release of granulocytes from bone marrow
fast mobilization causes
increased immature cells - left shift
neutrophilia means
bacterial infections
lymphocytophilia means
viral infections
eosinophilia menas
allergies and parasitic infections
other systemic effects besides fever
inc. HR and BP
decreased heat loss
shiver, chills, anorexia, sleepiness
what causes septic shock
high levels of bacterial products induce large amounts of cytokines (TNF, IL-1)
this causes hypotensive shock, blood clot disorders
what is secondary amyloidosis
prolonged production of SAA leads to deposits of misfolded SAA proteins
causes tissue disfunction
AA metabolites can be pro or anti inflammatory
true
IL-17 is important in neutrophil recruitment
true
T cells are the principle source of all but which mediator
IL-1
the production of CRP is stimulated by IL-1
false