Inflammation, immune complex-mediated

Fig. 2. IgG-mediated systemic versus local anaphylaxis, a IgG-mediated systemic anaphylaxis. When allergen-IgG immune complexes are formed in the circulation, basophils immediately capture them through IgG receptors on their surface and are activated to release PAF, that in turn act on vascular endothelial cells, leading to increased vascular permeability, b Passive cutaneous anaphylaxis. When allergen-IgG immune complexes are formed in the skin, they stimulate tissue-resident mast cells to release chemical mediators such as histamine, leading to local inflammation. 

Type III IgM, IgG complexed with antigen (immune complexes) leading to inflammation Type IV T-cell-mediated delayed-type hypersensitivity... 

Jatrorrhizine was found to possess anti-inflammatory activity as measured in the cobra venom factor-induced (CVF) rat paw edema. CVF edema was used to examine jatrorrhizine and other substances in order to detect novel compounds, since it has been shown that joint cyclooxygenase and lipoxygenase inhibitors, as well as immunoreactive drugs, exhibit more pronounced inhibitory effects on CVF in comparison to carrageenin-induced edema. CVF edema is dependent on activation of the complement system which plays an important role in acute and chronic inflammatory reactions, mediating the activity of immune complexes. This test system represents a functionally new type of acute inflammation via activation of the alternative complement pathway [290]. 

Thus complement is one of the major mediators of inflammation. Secondary edema and stasis permit the passage of further antibody, complement, and phagocytes into the extravascuiar space, aiding in the killing and removal of infectious agents and immune complexes. At the same time, thrombosis as a result of the secondary activation of platelets and the coagulation factors helps to localize infection. 

HP is characterized by diffuse inflammation of lung parenchyma and airways. There is controversy regarding the mechanisms of the immune response. Both humoral (type III) and cell-mediated (type IV) immune responses seem to play a role in pathogenesis (Salvaggio andMiLHOLLON 1993). They are mediated by immune complexes and Thl cells, respectively. 

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