| A | B |
|---|
| plasmin | proteolytic enzyme present in inflammatory exudate |
| kinninogens | vasoactive peptides generated from plasma proteins by kallikreins |
| bradykinin | vasoactive nonpeptide |
| effects of bradykinin | increased vascular permeability |
| Hageman's Factor | FACTOR XII of intrinsic clotting pathways |
| cleaves glycoprotein precursor,"high molecular weight kinniogen," to produce bradykinin | kallikrein |
| alternative pathway | cleavage of C3 in response to endotoxin, microbial LPS...cobra venom,etc... |
| C3 convertase | splits C3 to C3a and C3b |
| C3b | functional fragment of C3; covalently attaches to complement target; then to other c-fragments to form C5-convertase |
| C5-convertase | cleaves C5 to C5b and C5a; binds late components C6-9 together to form MAC |
| C5a activates | lipoxygenase pathway of arachidonic acid met. in PMNs and Monocytes |
| C5a | powerful chemotactant for neutrophils, monocytes, eoisinophils, basophils |
| C3b, iC3b | opsonins, fix to bacterial cell wall, enhance affinity for phagocytosis |
| PARs (protease activated receptors) | GPCRs on platelets, endothelialsm. muscle; bind various trypsin like serine proteases |
| engagement of PAR-1 by factor IIa triggers... | mobilization of P-selectin; prod. chemokines, PAF, NO, prostaglandins; |
| major coagulation protease, cleaves circulating soluble fibrinogen to... | thrombin; ...form insoluble fibrin clot |
| thrombin (factor IIa) | protease; main link between coagulation and inflammation |
| kallikrein | potent activator of Hageman Factor; autocatalytic amplification of initial stimulus |
| kallikrein | directly converts C5 to chemotractant C5a |
| effects of complement activation | increase opsonation, chemotaxis, vascular permeability, proteolytic enzymes |
| lectin pathway | plasma mannose bindinig lectin binds carbs on microbes--> C1 |
| VASOCONSTRICTION | thromboxane A2; leukotriense C4, D4, E4 |
| VASODILATION | PGI2, PGE1, PGE2, PGD2 |
| CHEMOTAXIS; LEUKOCYTE ADHESION | Leukotriene B4; HETE, lipotoxins |
| Prostaglandins, NO, Histamine | VASODILATION |
| Increased Vascular Permeability | Vasoactive Amines, Bradykinin; C3a, C5a; PAF, leukotrienes C4,D4,E4 |
| chemotaxis, leukocyte recruitment/activation | C5a; leukotrienes B4; chemokines; IL-1; TNF;prostaglandins |
| Pain | prostaglandinis; bradykinin |
| tissue damage | lysosomal enzymes from MACS & PMNs; ROS, NO |
| chemokines | increased avidity of integrins |
| leukocyte diapedesis; vascular permeabilty | predominantly in venules; capillaries of lungs |
| 1st 6-24 hours of inflammatory infiltrate | neutrophils predominate |
| hours 24-48 of inflammatory infiltrate | monocytes predominate |
| pre-formed, chemical mediators of inflammation in secretory granules | HISTAMINE; SEROTONIN; LYSOSOMAL ENZYMES |
| sources of pre-formed mediators in secretory granules | MCs; basophils; platelets; PMNs, Macs |
| cellular; newly synthesized chemical mediators of inflamm. | prostaglandins; leukotrienes; PAF; ROS; NO; Cytokines |
| source of synthesized cellular | allleukocytes, platelets, EC, Macs, No, Cytokines, Macs, lymphocyres |
| chemical mediators of inflam. from liver/plasma; Factor XII activation | Kinin System (bradykinin) |
| chemical mediators of inflam. from liver/plasma/complement activation; anaphalotoxin | C3a; C5a |
| chemical mediators of inflam. from liver/plasma/complement activation; membrane attack complex | C3b; C5b-C9 |
