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IF连续增长的期刊MEDIATORS OF INFLAMMATION Flashcards -
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&&&MEDIATORS OF INFLAMMATION
Mediators Of Inflammation
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62 Cards in this Set
Mechanisms of action of chemical mediators of inflammation
-Bind to receptors on target cells-Direct enzymatic activity (e.g. lysosomal proteases)-Oxidative damage (oxygen metabolites)
lifespan of mediators
short-lived, but can do damage if not adequately controlled
the hallmark of acute inflammation
Neutrophils: release many mediators of inflammation, stored in their granules
3 steps involved in Leukocyte extravastion?Requires activation of what?
ROLLING, ADHESION, DIAPEDESISrequires activation of both: The Leukocyte and endothelium
Preformed mediators in secretory granules (Cellular Mediators)
HISTAMINESEROTONINLYSOSOMAL ENZYMES
Newly Synthesized mediators of inflammation(Cellular Mediators)
PROSTAGLANDINSLEUKOTRIENESPLATELET-ACTIVATED FACTORSACTIVATED OXYGEN SPECIESNITRIC OXIDECYTOKINES
Examples of mediators in plasma
FACTOR XII ACTIVATION:bradykinin, coagulation/fibrinolysis systemCOMPLEMENT ACTIVATION:anaphylatoxins (C3a, C5a), C3b, C5b-9 (MAC)
Histamine:synthesized by:stored in:
synthesized and stored in mast cells in CT, adjacent to blood vessels, also found in circulating basophils, platelets
histamine is released in response to what?
-physical stimuli-immune reactions (x-linking of surface bound IgE)-anaphylatoxins (C3a, C5a)-cytokines (IL-1, IL-8)
release of histamine leads to what?(effects are through what receptors?)
dilation of arterioles, increased vascular permeability(effects on small vessels are through H1 receptors)
Serotonin (stored where?)
stored in platelets
Serotonin released by what?
released by platelet aggregation induced by collagen contact, thrombin, ADP, Ag-Ab complexes
Actions of Serotonin
actions, similar to histamineincreased vascular permeability
system of functionally linked proteins that interact with one another in a highly regulated manner to provide many of the effector fucntions of humoral immunity and inflammation
COMPLEMENT
examples of Complement mediated inflammatory actions
CYTOLYSIS by formation of the MAC, opsonization of foreign organisms, solubilizaztion and clearance of Ab-Ag complexes
In Classical pathway, complement is inactive in plasma until activated at localized sites by:
activated at localized sites by:Ag-Ab complexes
In Alternative pathway, pathway, complement is inactive in plasma until activated at localized sites by:
activated at localized sites by:surfaces of pathogens
central component of Complement Cascade
C3 is central componentboth pathways generate different C3 convertase complexes that activate C3, converting it to C3a and C3b
C3b action
proteolytically cleaves C5; C5b + C6, C7, C8 C9 ---& C5-9 (MAC)can also opsonize bacteria
C3a and C5a
anaphylatoxins, many of their actions are histamine dependentbind to mast cells and release histamine, causing dilation of arterioles, increased vascular permeability of the venules (histamine is the principal mediator of immediate vascular permeability)
Histamine independent actions of C5a:
-activates lipoxygenase pathway in PMN--& leukotrienes--& + permeability-potent chemoattractant for and activator of PMNs-increases leukocyte adhesion to endothelium
EICOSANOIDS
formed rapidly, local effects, short lived
where are eicosanoids formed?
formed in LIPID BODIES (specialized cellular domains, that have high concentration of the synthetic enzymes)
COX pathway-Initiated by:Results in:
Initiated by COX-1 or COX-2Results in: formation of PROSTAGLANDINS
Tissue restricted enzymes involved in arachidonic acid cascade
IN PLATELETS:
TxA2 synthase (makes TxA2 = vasoconstrictor)IN ENDOTHELIUM: Prostacyclin synthase (makes PGI2= a vasodilator)
Diapedesis
“the passage of blood, or any of its formed elements, through the intact walls of blood vessels.”eg:Leukocytes have to get out of the blood vessels and into the interstitium.
chemokine responsible for initial "rolling"
in leukocyte extravasation
SELECTINS expressed by endothelial cells, interact with glycoproteins on leukocyte to slow it downcooperates with Integrin-ICAM interaction in "STICKING" adhesion
chemokines activate what structure on leukocyte surface, that is primarily responsible for diapedesis?
INTEGRIN: on Leukocyte surface aids in establishing stable adhestion "STICKING" (along with selectin)and mediates migration through endothelium
chemokines
superfamily of small proteins that activate and chemoattract leukocytes
important characteristics of complement
-multiple proteolytic enzymes-sequential activation-amplification-highly regulated
complement is inactive until activated by:
-Ag-Ab complexes "Classical pathway"-Surfaces of pathogens "Alternative Pathway"
Effector Functions of Activated Complement
C3a C5a: INFLAMMATIONC3b: Opsonization/PhagocytosisC3b cleaves C5--& C5-9 (MAC): Lysis of Microbe
C3b proteolytically cleaves C5C5b + C6, C7, C8, C9 --& C5-9
Histamine dependent actions of anaphylatoxins
-bind to mast cells and release histamine-dilation of arterioles-increased vascular permeability of the venules
principal mediator of immediate vascular permeability
Factor XIIa induces what two cascades? Both these cascades interact and induce what downstream cascade?
Kinin cascade and Clotting Cascadeboth lead (indirectly) to activation of complement cascade
how do steroids exert their anti-inflammatory properties?
inhibit phospholipases that liberate arachidonic acid from cell membrane phospholipids
how do COX-1 and COX-2 inhibitors exert their anti-inflammatory properties?
inhibit cyclooxygenase involved in the conversion of ARACHIDONIC ACID to Prostaglandin G2 (PGG2)
PGI2 causes:opposes action of?
causes vasodilation, inhibits platelet aggregationopposes action of TxA2
TXA2 action:opposes action of what?
causes vasoconstriction, promotes platelet aggregationopposes action of PGI2
5-Lipoxygenase
Neutrophil specific enzymeinvolved in branch of arachidonic acid cascade that generates various Lipoxins, and Leukotrienes (some pro-, some anti-inflammatory
Products of Arachidonic Acid Cascade
EICOSDINOIDSformed in specialized cellular domains called lipid bodies, that have high concentration of synthetic enzymes
examples of eicosanoid metabolites involved in:-&vasoconstriction:
TxA2, LTC4, D4, E4eicosanoid metabolites involved in what action:
examples of eicosanoid metabolites involved in:-&vasodilation
PGI2, E1, E2, D2eicosanoid metabolites involved in what action:
examples of eicosanoid metabolites involved in:-&+ vascular permeability
LTC4, D4, E4eicosanoid metabolites involved in what action:
examples of eicosanoid metabolites involved in:-&chemotaxis, leukocyte adhesion
LTB4, HETE, Lipoxins
chemokines are secreted and bind to what?
cell surface proteoglycans (immobilized to form gradients)bind to 7transmembrane receptors and activate --& G PROTEINS
NO is released from what type of cells?
Endothelial cells
NO action on vessels
vasodilator
NO action as hormone
local paracrine factor
NO lifespan
SHORT LIVED
Importance of NO in host defense
can be used for killing of intracellular bacteria
IL1/TNF cytokines produced by
MACROPHAGE (and other cell) activation by: bacterial products, immune complexes, toxins, physical injury and other cytokines
IL1/TNF induced ACUTE-PHASE REACTIONS
fever+ sleep- appetite+ Acute phase proteinshemodynamic effects (shock)neutrophilia
IL1/TNF induced ENDOTHELIAL EFFECTS
+ Leukocyte adherence+ PGI synthesis+ Procoagulant activity- anticoagulant activity+ IL1, IL8, IL6, PDGF
IL1/TNF induced FIBROBLASTS EFFECTS
+ proliferation+ collagen synthesis+ collagenase+ protease+ PGE synthesis
IL1/TNF induced LEUKOCYTE EFFECTS
+ cytokine secretion (IL-1, IL-6)
chemokine specificity-eotaxin attracts what?whereas-IL-8 attracts what?
eotaxin attracts EOSINOPHILSIL-8 attracts NEUTROPHILS
Stimuli that activate NF-kB
TNFalphaIL-1betaLipopolysaccharide
Genes/proteins that are induced by NF-kB
TNFalphaIL-1beta
NFkappaB activation by LBP and CD14 involves what type of receptor?
TLR4TOLL LIKE RECEPTOR 4
aspirin can inhibit inflammation via COX inhibition and also through what action on NFkappaB pathway
inhibits IkB kinases (responsible for degradation/activation of NFkB and release of transcription factors)
Ready To Get Started?科研成果 - 我院肖诚研究员的论文发表在MEDIATORS OF INFLAMMATION - 中日友好医院
我院肖诚研究员的论文发表在MEDIATORS OF INFLAMMATION
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我院肖诚研究员以通讯作者身份撰写的论文“Triptolide Inhibits Osteoclast Differentiation and Bone Resorption In Vitro via Enhancing the Production of IL-10 and TGF-beta 1 by Regulatory T Cells”于2016年6月份发表在MEDIATORS OF INFLAMMATION，影响因子3.236。& & & & & & & & & & & & & & & & & & & & & & & & & & & & & & & & & & & & & & &科研处& & & & & & & & & & & & & & & & & & & & & & & & & & & & & & & & & & & & & 日}