Immune Dysfunctions and Abrogation of the Inflammatory Response by Environmental Chemicals.
Abstract
During the past year we have further characterized the immunotoxic effects of 1,1-dimethylhydrazine (UDMH). Evidence has been accumulated which indicates that UDMAH interferes with the regulatory arm of the immune system at low dose or concentration levels. Results from earlier experiments which supported this conclusion included: increased Jerne plaque response in UDMH-treated mice; abrogation of concanabalin A-induced suppressor activity following in vivo or in vitro UDMH exposure; and enhancement of lymphocyte blast transformation (LBT) by UDMH-treated lymphocytes. During the past year we have shown that at least one type of regulatory cell which UDMH appears to inhibit is in the adherent cell population of splenocytes. This is demonstrated by the fact that exposure of adherent cells to UDMH enhanced the mixed lymphocyte reaction (MLR). Preliminary experiments now in progress indicate that the UDMH suppresses prostaglandin E (PGE) production by the adherent splenocyte population, which would explain the effects seen in the MLR, as PGE has been shown by others to inhibit various immune responses, including the MLR. Experiments are currently underway which will evaluate the effects of UDMH on PGE synthesis by various subpopulations of lymphocytes and macrophages, as well as on cyclic nucleotide levels and Ia antigen expression (Ia antigen is a product of the immune responder genes). (Author)
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 1982
- Accession Number
- ADA121800
Entities
People
- Richard G. Olsen
Organizations
- Ohio State University