Pharmacology of Inflammation Flashcards
increase vascular permeability, bronchoconstriction
leukotrienes
prostaglandins class
lipid mediators
increased extracellularly during injury: anti-inflammatory, inhibit cytokine action
adenosine
glucocorticoids cellular source
adrenal cortex
bradykinin cellular source
endothelial cells
bradykinin class
peptide
Oxygen-derived free radicals class
superoxide, hydroxy radicals
vasodilation, pain, fever, platelet aggregation (via thromboxane)
prostaglandins
cell adhesion molecules mechanism
contact molecules, calcium dependent
prostaglandins mechanism
activation of specific GPCRs
adenosine cellular source
all cells
leukotrienes mechanism
activation of GPCRs
glucocorticoids class
lipid mediators
prostaglandins cellular source
virtually all cells
complement system cellular source
synthesized by liver, circulate in blood
C-reactive protein class
plasma proteins
Histamine cellular source
mast cells, basophils
complement system mechanism
complement protein complexes cause osmotic lysis activation of GPCRs
C-reactive protein cellular source
produced in liver in response to cytokines, also produced in adipocytes
cell adhesion molecules cellular source
endothelial cells, platelets, leukocytes
leukotrienes cellular source
macrophages, neutrophils
cytokines mechanism
bind to specific receptor proteins to induce gene expression of number of proteins via activation of Nf?B and AP-1; increase COX (fever) and lipoxygenases, increase adhesion molecule expression, induce collagenase (fibrosis)
inhibition of cytokines, inhibition of phospholipase A2, inhibition of COX-2, inhibition of cell adhesion molecules
glucocorticoids
vasodilation, increased vascular permeability, pain
histamine
cytokines class
secreted proteins, in particular the pro-inflammatory cytokines: Interleukin-1 (IL-? & IL-?) and TNF-?
vasodilation, increased microvessel permeability, pain
bradykinin
cell adhesion molecules class
family of proteins
histamine class
biogenic amine
Acute-phase reactant, activates complement cascade, mediates phagocytosis, marker of inflammation
C-reactive protein
Histamine mechanism
activation of GPCRs
adenosine mechanism
activation of GPCRs
cytokines cellular source
nearly all inflammatory cells
glucocorticoids mechanism
activation of nuclear receptors
intracellular killing of bacteria by neutrophils
Oxygen-derived free radicals
chemotaxis, promote release of mediators from neutrophil, increase vascular permeability, excessive activation may contribute to tissue injury
complement system
Oxygen-derived free radicals cellular source
all cells
Oxygen-derived free radicals mechanism
protein oxidation, lipid peroxidation, DNA mutations
leukocyte adhesion to endothelium is a pivotal event in host defense and tissue repair, endothelial adhesion molecules contribute to recruitment of activated platelets
cell adhesion molecules
bradykinin mechanism
activation of GPCRs
TNF-?: acute phase reaction, fever, sepsis; IL-1: acute phase reaction, fibroblast, and lymphocyte proliferation, fever
cytokines
leukotrienes class
lipid mediators
adenosine class
purine nucleoside formed from breakdown of ATP
complement system class
plasma proteins
C-reactive protein mechanism
bind to phospholipids in bacteria and damaged cells may be specific receptors in macrophages