title: Role of glucocorticoids in ethanol-induced decreases in expression of MHC class II molecules on B cells and selective decreases in spleen cell number.
abstract: Glucocorticoids have been implicated in some of the immunosuppressive effects associated with acute ethanol (EtOH) intoxication, but other neuroendocrine mediators that are induced by EtOH can also be immunosuppressive. The possibility that glucocorticoids may act additively or synergistically with other mediators to produce immunosuppression has not been fully investigated. In the present study, complementary methods were used to address this issue. EtOH dose-responsively decreased the following parameters in the spleen in B6C3F1 mice: total cell number, mature B cell (IgM+IgD+) number, and expression of MHC class II molecules on B cells. These effects were most pronounced 12 hr after administration of EtOH. The glucocorticoid antagonist, RU 486, completely or partially blocked these effects. Thus, glucocorticoids seem necessary for full expression of these immunological changes in EtOH-treated mice. To determine if glucocorticoids are also sufficient to cause these effects, corticosterone was administered to achieve serum levels and kinetics comparable to those in EtOH-treated mice. This decreased the expression of MHC class II molecules on B cells to the same extent as treatment with EtOH. However, the other parameters were not affected by administration of corticosterone. Thus, corticosterone is necessary and sufficient to decrease expression of MHC class II molecules on splenic B cells, but other mediators in addition to corticosterone are required to decrease total spleen cell number and the number of mature B cells in the spleen.
authors.affiliation: Department of Biological Sciences, Mississippi State University, 39762, USA.
authors.forename: P A
authors.initials: PA
authors.lastname: Weiss
authors.forename: S D
authors.initials: SD
authors.lastname: Collier
authors.forename: S B
authors.initials: SB
authors.lastname: Pruett
mesh_terms: D000021:Abortifacient Agents, Steroidal / Q000633:toxicity; D000704:Analysis of Variance; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000633:toxicity; D001402:B-Lymphocytes / Q000166:cytology / Q000187:drug effects* / Q000276:immunology; D002452:Cell Count / Q000187:drug effects; D002492:Central Nervous System Depressants / Q000633:toxicity*; D003345:Corticosterone / Q000097:blood / Q000633:toxicity; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000633:toxicity*; D005260:Female; D005434:Flow Cytometry; D005786:Gene Expression Regulation / Q000187:drug effects / Q000235:genetics; D005938:Glucocorticoids / Q000037:antagonists & inhibitors / Q000502:physiology*; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis*; D007166:Immunosuppressive Agents / Q000633:toxicity*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D015735:Mifepristone / Q000633:toxicity; D013047:Specific Pathogen-Free Organisms; D013154:Spleen / Q000166:cytology / Q000187:drug effects / Q000276:immunology
chemical_list: D000021:Abortifacient Agents, Steroidal; D000893:Anti-Inflammatory Agents; D002492:Central Nervous System Depressants; D005938:Glucocorticoids; D000949:Histocompatibility Antigens Class II; D007166:Immunosuppressive Agents; D015735:Mifepristone; D000431:Ethanol; D003345:Corticosterone