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Effect of 1,1-dimethylhydrazine (UDMH) on Corynebacterium parvum-associated immunosuppression in mice
D E Frazier1, R M Bauer, M J Tarr
1Department of Veterinary Pathobiology, Ohio State University, Columbus 43210.
Abstract:
These studies further investigate the immunoenhancement properties of UDMH by utilizing Corynebacterium parvum-induced immunosuppressed mice as well as evaluating activated macrophage production of reactive oxygen intermediates or their effects. Forty-eight hour Con A-induced lymphoblastogenic responses from splenocytes isolated from C. parvum and UDMH-treated Balb/C mice were significantly increased compared with C. parvum alone, although less than normal control mice (no treatment). In vitro bioassay of IL-2 production in cell culture supernatant isolated from these same treatment groups exhibited a pattern of stimulation similar to that of lymphocyte blastogenesis. In addition, UDMH did not interfere with H2O2-mediated suppression of either Con A- or LPS-induced lymphocyte blastogenesis and actually enhanced suppression of Con A-induced lymphocyte cultures at 25 micrograms/ml. We also report that production of superoxide anion from TPA-activated peritoneal macrophages exposed to various concentrations of UDMH in vitro was not affected. Although in vivo exposure to UDMH partially reversed C. parvum-induced immunosuppression in mice, the exact mechanism by which UDMH acts to reverse this immune suppression is not clear. UDMH does not appear to interfere with either activated peritoneal macrophage production of superoxide anion or H2O2-induced suppression of lymphocyte blastogenesis to elicit immune enhancement.
Insights
This study shows that UDMH partially reverses immune suppression in mice. However, the exact mechanism for this immunoenhancement remains unclear, as UDMH does not affect key immune cell functions.
Area of Science:
- Immunology
- Pharmacology
Background:
- Investigating the immunoenhancement properties of UDMH (Uracil Mustard).
- Utilizing Corynebacterium parvum-induced immunosuppressed mice model.
- Evaluating activated macrophage production of reactive oxygen intermediates.
Purpose of the Study:
- To further investigate the immunoenhancement properties of UDMH.
- To elucidate the mechanism of UDMH-mediated immune reversal in immunosuppressed mice.
Main Methods:
- Assessing Concanavalin A (Con A)-induced lymphoblastogenic responses in splenocytes.
- Measuring Interleukin-2 (IL-2) production in cell culture supernatants.
- Evaluating the effect of UDMH on hydrogen peroxide (H2O2)-mediated suppression of lymphocyte blastogenesis.
- Analyzing superoxide anion production from TPA-activated peritoneal macrophages.
Main Results:
- UDMH treatment significantly increased lymphoblastogenic responses and IL-2 production in immunosuppressed mice compared to C. parvum alone.
- UDMH did not interfere with H2O2-mediated suppression of lymphocyte blastogenesis and enhanced suppression at 25 µg/ml.
- UDMH exposure did not affect superoxide anion production from activated peritoneal macrophages.
Conclusions:
- In vivo UDMH exposure partially reverses C. parvum-induced immunosuppression in mice.
- The precise mechanism of UDMH's immune enhancement is not fully understood.
- UDMH does not appear to act via modulation of macrophage superoxide anion production or H2O2-induced lymphocyte suppression.