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RECORD NUMBER: 29 OF 72

OLS Field Name OLS Field Data
Main Title Glucocorticoid Effects on Natural and Humoral Immunity in Mallards.
Author Fowles, J. R. ; Fairbrother, A. ; Fix, M. ; Schiller, S. ; Kerkvliet, N. I. ;
CORP Author Oregon State Univ., Corvallis. Coll. of Veterinary Medicine. ;ManTech Environmental Technology, Inc., Corvallis, OR.;Corvallis Environmental Research Lab., OR.
Publisher c1993
Year Published 1993
Report Number EPA/600/J-93/205;
Stock Number PB93-199644
Additional Subjects Antibody formation ; Natural killer cells ; Glucocorticoids ; Ducks ; Pharmacology ; Dexamethasone ; In vitro analysis ; Lymphocytes ; Phagocytosis ; Immunologic cytotoxicity ; Indomethacin ; Macrophages ; Blood chemical analysis ; Prostaglandins ; Hematology ; Reprints ;
Holdings
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Status
NTIS  PB93-199644 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. NTIS 08/23/1993
Collation 15p
Abstract
Adult male mallards were treated with dexamethasone (DEX) to observe the impact of glucocorticoids (GC) upon natural killer cell activity, humoral antibody response to sheep erythrocytes (SRBC), and other physiologic parameters. Results showed that DEX caused significant decreases in total and 2-mercaptoethanol-resistant antibody responses, while a separate experiment showed that DEX resulted in consistent elevation of NKC activity. In-vitro studies showed that DEX and indomethacin were protective of NKC activity in the presence of monocytes, and that prostaglandin-E2 was highly suppressive when added to non-adherent NKCs. Furthermore, DEX caused only a slight loss in lymphocyte viability in-vitro at 10 to the minus fifth M but significantly reduced phagocytic ability of mature monocytes. From these results, mallard lymphocytes and NKC activity appear refractory to glucocorticoid-mediated suppression, and it is suggested that the elevation in activity observed is likely due to an inhibition of prostaglandin production by monocytes.