Glutaraldehyde has a wide spectrum of uses which can result in dermal contact with the agent. The low number of reports of hypersensitive reactions to glutaraldehyde indicates a low incidence of sensitization. This paper describes the contact hypersensitivity response to glutaraldehyde in the guinea pig and the mouse. Female albino Hartley strain guinea pigs and female B6C3F1 mice were sensitized with 0.3, 1.0 and 3.0% glutaraldehyde and challenged with 10% glutaraldehyde. Doses of glutaraldehyde were selected from assays for primary irritancy. Guinea pigs received 100 microliters by direct dermal application, for 14 consecutive days, and mice received 20 microliters by direct dermal application, for 5 or 14 consecutive days, to sites prepared by shaving and dermabrading. Rest periods were 7 or 14 days for guinea pigs and 4 or 7 days for mice. Measurement of the contact hypersensitivity response in guinea pigs was both visual evaluation (scoring) at 24 and 48 hours following challenge and radioisotopic assay at 48 hours, and in mice by radioisotopic assay 48 hours after challenge. Both guinea pigs and mice demonstrated dose-dependent contact hypersensitivity responses to glutaraldehyde. The radioisotopic assay appeared to be more sensitive than visual evaluation in detecting contact allergic hypersensitivity to glutaraldehyde.
The effects of pentachlorophenol (PCP) on selected parameters reflecting immunocompetence of female B6C3F1 mice were measured following subchronic exposure (14 d) and direct exposure in culture. Daily exposure was by gastric intubation of 10, 30, or 100 mg/kg of technical-grade PCP (PCP-T), or 100 mg/kg of EC-7, a PCP preparation purified to reduce contamination (PCP-P), or 100 mg/kg of the vehicle, corn oil. There were no effects on the antibody responses of spleen-cell suspensions from either PCP-T- or PCP-P-treated mice stimulated with antigen in culture. In contrast, when mice were immunized during the exposure to PCP-T, there was a dose-related suppression of the IgM antibody response to sheep red blood cells (SRBC) measured on both d 4 (peak day) and d 5. There was no change in the antibody response of mice exposed to PCP-P. The differential activity was not observed following direct addition, since both PCP-T and PCP-P suppressed the in vitro antibody response by spleen-cell suspensions from untreated mice. The suppression was associated with a decrease in cell viability, indicating that both preparations were directly cytotoxic. These results indicate that the in vitro antibody assay will be of limited value in determining the mechanism of immunosuppression by PCP. The lack of effect on the antibody response by splenocytes from PCP-T-treated mice indicates that the dysfunction is not due to a direct suppression of the capabilities of immunocompetent cells.
The macrolide antibiotic, clarithromycin, is used extensively to treat bacterial infections associated with pneumonia, duodenal ulcers, and the advanced stages of human immunodeficiency viral (HIV) infection. In addition to its antimicrobial properties, several studies have indicated that clarithromycin also has anti-inflammatory and immunomodulatory properties. In this study, clarithromycin's immunomodulatory properties were evaluated using female B6C3F1 mice and a panel of immune assays that were designed to evaluate potential changes in innate, and acquired cellular and humoral immune responses. Female B6C3F1 mice were treated daily by gavage with clarithromycin (0, 125, 250, and 500 mg/kg) for 28 days then evaluated for immunomodulation. Minimal immunological changes were observed after 28 days of treatment. A slight increase in the number of spleen antibody-forming cells was observed at the 250 mg/kg treatment level, but not at other doses. Serum IgM levels were unaffected by the clarithromycin treatment. A significant increase in the number of splenic macrophages was also observed in mice treated with 125 mg/kg of clarithromycin, but this increase was not observed at the other treatment levels. Innate and cell-mediated immunity, as measured by natural killer cell activity, and mixed leukocyte and cytotoxic T cell response, respectively, were unchanged following treatment with clarithromycin. These results suggest that the immune system is not a target for clarithromycin at doses of 500 mg/kg or below.
para-Nitrotoluene (p-nitrotoluene) is used primarily as an intermediate in the production of various dyes, explosives, pharmaceuticals, and in the production of rubber and agricultural products. Previous investigations indicated that p-nitrotoluene was mutagenic in the Ames Test and that other mono-substituted nitrotoluenes bound covalently to hepatic macromolecules. The objective of these studies was to evaluate the potential immunotoxicity of p-nitrotoluene in mice exposed by the oral route. Mice exposed to p-nitrotoluene (200-600 mg/kg) daily for 14 days showed modest dose-dependent increases in liver and spleen weights. The livers of mice exposed subchronically to 400 and 600 mg/kg showed a mild to moderate swelling of the hepatocytes adjacent to the central veins; this swelling appeared to be reversible and there was no evidence of necrosis. The proportion of monocytes in blood was decreased in mice treated with p-nitrotoluene or toluene. Serum chemistries, bone marrow cellularity and the number of CFU-M and CFU-GM were unaffected. Immunologic investigations showed p-nitrotoluene suppressed the IgM response to sRBC and the DHR response to KLH. There was a 24% decrease in the percentage of CD4+ T lymphocytes in the spleen. There was no dose-dependent alteration of peritoneal macrophage numbers or differential count, unstimulated natural killer cell activity, response to B cell mitogen LPS, C3 activity or interferon levels. Exposure of mice to p-nitrotoluene decreased resistance to Listeria monocytogenes but not to Streptococcus pneumoniae, Plasmodium yoelii or the B16F10 melanoma, and increased resistance to the PYB6 tumor. These studies indicated that the immune system is an important target for toxicity of p-nitrotoluene. The decreased host resistance to L. monocytogenes can be attributed to the decrease in T lymphocytes and to a decreased delayed hypersensitivity response to KLH.
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