Azoreductases from several anaerobic intestinal bacteria have been shown to reduce azo dyes to carcinogenic aromatic amines. To evaluate the structural similarities of azoreductases from four species of Clostridium and one species of Eubacterium, a polyclonal antibody against purified Clostridium perfringens azoreductase was generated in rabbits. This antibody inhibited the azoreductase activity of all five bacteria tested. ELISA showed different degrees of binding of the antibody to various species of bacteria. In a Western blot, the antibody reacted with the purified azoreductases from all four Clostridium species and the Eubacterium species. These results demonstrate that the azoreductases from the bacteria tested share similar antigenic domains, which are probably located in the active site of the enzyme. Azoreductases from these intestinal bacteria are similar enough to be considered as a single group of enzymes with respect to their functions and antigenicity.

This study was performed in female B6C3F1 mice to confirm previously observed effects of selected cephalosporin antibiotics on nonspecific immunity, and to determine possible effects on specific acquired immunity and host resistance. Mice were treated intravenously with DQ-2556, ceftizoxime or ceftezole at 800 mg/kg/day for 3, 5, or 7 consecutive days. All three compounds increased total serum IgM levels from day 3, but had no effects on total serum IgG levels and the thymus weight. All three cephalosporin antibiotics caused a slight increase in spleen weight and splenic germinal centers were enlarged after 5- or 7-day treatments. Antibody responses to type III pneumococcal polysaccharide (S3), a T-cell-independent immunogen, and sheep red blood cells (SRBC), a T-cell-dependent immunogen, were slightly decreased after 5-day dosings with each compound, and reached significance in DQ-2556 (response to S3) and ceftizoxime (response to S3 and SRBC). None of the tested cephalosporin antibiotics altered delayed-type hypersensitivity to oxazolone or host resistance to Plasmodiumyoelii, indicating that the antibiotic-treated mice retained the capacity to mount a multicomponent and sustained protective immune response. These data suggest that although cephalosporins may cause polyclonal expansion of B cells with associated increases in total serum IgM, they do not affect the tested measures of cell-mediated immunity or host resistance. The decreased IgM antibody responses to S3 and SRBC are associated with but not known to be causally related to the concurrent IgM hypergammaglobulinemia.

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