mediators of inflammation Flashcards
three stages of inflammatio
acute, subacute, chronic
what orchesrates inflammatory response?
mediators
pleiotropic
could have more than one response
cell derived mediatorys
vasoactive amines enzymes prostgladins cytokines + chemokines neuropeptides
plasma derived mediators
complement system
kinin system
coagulation (clotting) system
once mediatory released from the cell
short lived, decay quickly and inactivated or inhibited
vasoactive amines
preformed mediators
histamine- vasolidation, vascular permeabilty
(mast cells, basophils, platelts)
serotonin - vasoconctrstion
(platlets)
Leukocyte Lysosomal Enzymes
prefroemd mediators
secreted (elastase)- destroy and digest microbes
- destroyed phagocytosed substances
- casues tissue damage
(ex. elastase, collagenase, cathepsin)
newly synthesized mediators
AA
eicosanoids
20-carbn
cell membrane phospholipid coponets
mast cells, leukocytes endothelial cells
AA mechanism
power point
Newly Synthesized : PAF
phospholipid-derived mediator-- * aggregates platlets vasodialtion increased permeabilty chemotaxis
PAF mechanism
POwerpoint
cytokines
polypeptide products of many cell types
abudnatly produced by what?
macrohphage and lymphcoytes
action and effects of chemokines
autocrine
paracrine
endocrine
major cytokines in acute inflammation
TNF, Il-1, Il-6, chemokines
cytokines principle role is?
endothelial activation
chronic inflamation cytokines
Il-12 and IFN-y
chemikines
chemoattractants for leukocytes
function of chemokines
leukocyte recruitment
control cellular organization
activate leukocytes
classification
cxc chemokines
Il-8 ==> acute
classification cc chemokines
Mcp, mip rantes==>chronic
chemokines regulate?
cell trafficking
cells migrate toward during chemotaxis to?
toward higher concentraion of chemokines
neuropeptides
play a role in
pain, regulate vessel tone
vascular permeabilty
Calcitonin Gene Related Peptide
vasodialtion
transmit pain signals
what releases ROS
activated pmns and macrophages
lysosomal ros
destroy phagocytosied microbes and necrotic cellls
secreted ros low levels
^ chemokine, cytokine, adhesion molecule
secretied ros high levels
endotheial damage, ^ permeabilty
direct cell injury
NO endothieal
eNOS (anti-inflammatory effects)
- vasoliation
- reduced adhesion
NO macrophage
iNOS
* cytotoxic
plasma protein derived mediators
Hageman Factor
complement
kinin
coagulation
how is inflammation turned off
short lived
endogenous
anti inflammator
pharmaceuticals
anti-inflammatory cytokines
iL-10-inhibts TNF
IL-2, IL-4 - promote repair
endogenous “anti” mediators
antioxidants, lipoxins, protease inhibits, resolvins
pharmaceuticals
nsaids (blocks cyclooxygenase (PG production
steroids - block PLA2 (aa formation)
Etanecceot - block action of TNF
antihistamines
plaque biofilm reases
toxins, cytokines (LPs, TNF, IL1,8, PGE2)
Periodontics
ongoing inflamamtion/infection (CRP, fibrinogen, Il-6)
Sysremic disease with oral health disease
cardiovascular disease
diabetes
COPD