It is now recognized that antibacterial agents, whose main target is the microorganism, may also interfere with host cell functions (8). The many studies which have been performed in vitro, ex vivo, and in vivo have raised the possibility that some antibacterial drugs may indeed alter the inflammatory response. It is well documented that ampicillin, penicillin G and various aminothiazolyl-cephalosporins possess oxidant-scavenging proper ties in vitro (9-11), although in vivo j3-lactam treatment may, on the contrary, enhance the inflammatory response in meningitis or lead to inflammatory sequelae, particularly in otitis. Recently, we demonstrated that OH-iminocephems directly inhibit myeloperoxidase in vitro (12,13), but no data are available on the in vivo effects of these drugs in inflammatory settings. Dapsone, clofazimine, and isoniazid also inhibit the myeloperoxidase system in vitro (14-15), and several authors have suggested that part of their therapeutic activity in mycobacterial diseases is linked to their anti-inflammatory potential. Finally, the ansamycins and the cy-clines have proved beneficial in various inflammatory settings not directly linked to infections.
For both kinds of drugs, the hypothesis underlying clinical trials was their cellular uptake property and bioactivity on several microorganisms suggested to play a role in the pathogenesis of rheumatoid arthritis. This hypothesis has not been substantiated, but clinical trials have shown that intraarticular rifamycin SV was beneficial in rheumatoid arthritis, ankylosing spondylitis, and juvenile rheumatoid arthritis (16-18). Similarly, cy-clines (particularly minocycline) have shown therapeutic benefit in reactive arthritis and mild to moderate rheumatoid arthritis (19-21). It must be noted that outside of their antibacterial activity these drugs have widely acknowledged effects on various inflammation mediators/effectors such as inhibition of neutrophil functions and oxidant-scavenging properties (ansamycins, cyclines) and inhibition of metalloproteinases and prostaglandin synthesis (cyclines). The question as to whether macrolides could attenuate inflammatory responses were raised about 25 years ago (22-24) (e.g., erythromycin and troleandomycin in asthma, chronic bronchitis, and other inflammatory settings). In the last 5 years, an explosion of clinical trials and fundamental research in vitro and in animal models has again put this new potential for macrolides on center stage.
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