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Factors released by platelets that lead to PMN and macrophage recruitment after injury
TGFbeta, PDGF
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Cell type instrumental in wound healing that release TGFbeta and PDGF, IL-1 and TNFalpha
Macrophages
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Factors released by endothelium after injury
Platelet-activating factor, tissue factor
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Growth factor that is chemotactic, activating for macrophages, PMNs and fibroblasts. Overproduction can cause fibrosis
TGF beta
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Growth factor that is chemotactic for PMNs, macrophages and fibroblasts. Has been shown to accelerate wound healing
PDGF
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Growth factors that are chemotactic for fibroblasts, though less potent than TGF beta (2)
EGF, FGF
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Chemotactic factors for inflammatory cells (7)
TGF beta, PDGF, IL-8, LTB-4, C5a and C3a, PAF
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Chemotactic factors for fibroblasts (4)
TGF beta, PDGF, EGF, FGF
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Angiogenic factors (6)
TGF beta, EGF, FGF, TGF alpha, IL-8, hypoxia
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Epithelialization factors (5)
TGF beta, PDGF, EGF, FGF, TGF alpha
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Length of time PMNs last in tissues
1-2d
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length of time platelets last in tissues
7-10d
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primary cell type in Type I hypersensitivity reactions
eosinophils
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factor released by eosinophils, causing basophils and mast cells to release histamine
major basic protein
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functions of histamine (3)
vasodilation, tissue edema, postcapillary leakage
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functions of bradykinin (4)
vasodilation, increased permeability, pain, contraction of pulmonary arterioles
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molecule that activates guanylate cyclase and increases cGMP, resulting in vascular smooth muscle dilation
NO
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Hormone that causes vascular smooth muscle constriction
Endothelin
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Cytokine produced largely by macrophages, a procoagulant, and causes cachexia in cancer patients
TNF alpha
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Cytokine that activates PMNs and macrophages, causes fever, hypothermia, tachycardia
TNF alpha
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Cytokine produced largely by macrophages, responsible for fever, increases IL-6
IL-1
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Cytokine that increases hepatic acute phase proteins
IL-6
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Cytokines released by lymphocytes in response to viral infection; activate macrophages, NK cells and cytotoxic T cells to inhibit viral replication
Interferons
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Cell adhesion molecules on leukocytes that bind ICAMs
Beta-2 integrins
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Cytokines that mediate early loos adhesion, or cell "rolling" for PMN activation
Selectins
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Complement pathway activated by antigen-antibody complexes
Classic pathway
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Complement factors found only in the classic pathway (3)
C1, C2, C4
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Complement pathway activated by endotoxin, bacteria
Alternative pathway
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Complement factors found only in alternative pathway
B, D, and P
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Complement factor common to both classic and alternative pathway, and is the convergence for the two
C3
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Anaphylatoxins that increase vascular permeability and activate mast cells and basophils
C3a, C4a, C5a
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Membrane attack complex components
C5b-C9
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Complement factor that is important for opsonization
C3b
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Complement factor important for chemotaxis
C3a, C5a
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Prostaglandins for vasodilation, bronchodilation, increased permeability, and platelet inhibition
PGI2, PGE2
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Prostaglandin for vasodilation, bronchoconstriction, and increased permeability
PGD2
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Drugs that inhibit cyclooxygenases reversibly
NSAIDS
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Drug that inhibits cyclooxygenases irreversibly, and inhibit platelet adhesion by decreasing TXA2
aspirin
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drugs that inhibit phospholipase, which convert phospholipids to arachadonic acid
steroids
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slow reacting substances of anaphylaxis that cause bronchoconstriction, vasoconstriction followed by increased permeability
leukotrienes LTC4, LTD4, LTE4
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chemotactic leukotriene
LTB4
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Peak catecholamine response after injury
24-48 hours
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neural response to injury
epi and norepi release
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origin of norepinephrine release after injury
sympathetic postganglionic neurons
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origin of epinephrine release after injury
adrenal medulla
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factors released as neuroendocrine response to injury
CRF, ACTH, ADH, Growth hormone
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Role of CXC chemokines (3)
Chemotaxis, angiogenesis, wound healing
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Oxidants generated in inflammation (5)
Superoxide anion, hydrogen peroxide, hydroxyl radical, hypochlorous acid, chloramines
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Primary mediator of reperfusion injury
PMNs
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Defect in PMN NADPH-oxidase system resulting in decreased superoxide radical formation
Chronic granulomatous disease
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