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Prohost Modulation of Immunity by Isoprinosine and NPT 15392

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Abstract

Antimicrobial agents which act on nucleic acids (e.g., rifampin, sulfonamides, trimethoprim, metronidazole), on ribosomes (e.g., tetracyclines, chloramphenicol, aminoglycosides) or on cytoplasmic membranes (e.g., amphotericin B, griseofulvin, polymyxin, imidazoles) positively influence the outcome of infections by acting against the offending pathogens but they may also have negative effects on the host’s immunocompetence (22). Although the immunosuppressive properties of most of the antimicrobials are not sufficient to warrant restricting their use, under certain circumstances a “pro-host” immunopharmacological approach seems warranted. In this regard it is important to remember that the immune system “cures” an infection, not the antimicrobial agent, and under circumstances where antimicrobial therapy is lifesaving, the host’s immune defenses are almost invariably compromised. To expedite the development of immunorestorative therapy it is important first of all to characterize the immunological deficiency which precedes, accompanies or follows a disease in order to select the appropriate immunorestorative agent. Secondly, new therapeutic strategies, where the antimicrobials are associated with prohost immunomodulating drugs, need to be studied in the appropriate animal systems.

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DeSimone, C., Hadden, J.W. (1987). Prohost Modulation of Immunity by Isoprinosine and NPT 15392. In: Szentivanyi, A., Friedman, H., Gillissen, G. (eds) Antibiosis and Host Immunity. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1901-6_32

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