Neutrophils and monocytes are the prime defenders of the body against suppurative bacterial and fungal infections. To accomplish their role in inflammation, they must respond appropriately to chemotactic signals elaborated from complement and bacteria. This response predictably results in the adherence and subsequent directed movement of the phagocytes toward the infected area where they recognize opsonized microbes. Attachment of the microbes to the membrane of the cell leads to their ingestion and subsequent demise, principally by the reduced oxygen by-product H2O2, which is generated by the neutrophils and monoctyes during phagocytosis. Optimal killing requires the translocation of granule myeloperoxidase into the phagocytic vacuole containing the bacteria and a suitable halide ion. Degranulation is controlled, in part, by assembled microtubles whereas ingestion requires assembly of submembrane microfilaments. Deficiency states resulting from vitamin E results in dimished membrane-related chemotaxis and ingestion, whereas depletion of cellular GSH results in defective microtubule assembly preventing the normal increase in adherence, chemotaxis, degranulation, and microbicidal activity of the phagocytic cells. Deficiency states resulting in dysfunction of the microtubule system include neutrophil glutathione synthetase deficiency, rodent glutathione peroxidase deficiency, and the Chediak-Higashi syndrome.