Cefodizime stimulates subpopulations of cells mediating spontaneous or antibody-dependent cytotoxicity in patients with bacterial infections.
The influence of cefodizime (CDZ) on spontaneous cell-mediated cytotoxicity (SCMC) and antibody-dependent cell-mediated cytotoxicity (ADCC) was investigated in nine patients with conditions predisposing to infection (T-cell deficiency, humoral immune deficiency, myeloproliferative syndrome, kidney or liver damage, or chronic pulmonary disease). SCMC, using the K562 and LIK cell lines as targets, and ADCC, using the LIK cell line, were measured at baseline and after ten days of therapy with CDZ for lower respiratory tract infections. Six patients were cured; clinical outcome was not evaluable in the other three. SCMC lysis of K562 cells did not change significantly. SCMC and ADCC lysis of LIK (lymphoblastoid) cells both increased significantly. CDZ selectively stimulated a subpopulation of NK cells in this population of immunocompromised patients with lower respiratory tract infections.
Auer
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Medizinische Universitätsklinik Würzburg, Germany.
Hardörfer
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Zimmermann
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D000328:Adult; D000368:Aged; D000920:Antibody-Dependent Cell Cytotoxicity / Q000187:drug effects*; D001424:Bacterial Infections / Q000188:drug therapy / Q000276:immunology*; D002439:Cefotaxime / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D003602:Cytotoxicity, Immunologic / Q000187:drug effects*; D005260:Female; D006801:Humans; D007155:Immunologic Factors / Q000494:pharmacology*; D008297:Male; D008875:Middle Aged
D007155:Immunologic Factors; D002439:Cefotaxime; C033356:cefodizime