Immune complex-mediated drug-induced

Immune complex deposition, immediate hypersensitivity, direct drug toxicity, and induction of anti-tissue antibodies have all been suggested. Interleukin-6 may be an important mediator of trimethoprim-induced aseptic meningitis in some patients. A case with three episodes after re-exposure to co-trimoxazole has been reported (41). Polymorphonuclear or mononuclear cells may preponderate (42). Interleukin-6 may be an important mediator of trimethoprim-induced aseptic meningitis in some patients (43,44). 

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]. 

Type in hypersensitivity is mediated by soluble immune complexes mostly involving IgG antibodies. Drug-induced serum sickness-like reaction is the prototype example of type III drug hypersensitivity. Hypersensitivity vascu-Ms is another example of a type III hypersensitivity response induced by drugs. 

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