| Autor: |
Collier, Stephanie D., Wu, Wen-Jun, Pruett, Stephen B. |
| Zdroj: |
Alcoholism: Clinical & Experimental Research; 2000, Vol. 24 Issue 3, p291-299, 9p |
| Abstrakt: |
Background: Acute administration of EtOH suppresses basal NK cell lytic function in mice, and this suppression is caused, in part, by neuroendocrine mediators induced by EtOH. There is also evidence that a smaller part of the suppression is caused by direct action of EtOH. However, activation of NK cells to higher levels of lytic activity may be more important than basal NK cell lytic function in resistance to cancer or infectious agents. Therefore, the study described here examined the effects of acute EtOH exposure on activation of NK cells by polyinosinic-polycytidilic acid (poly I:C). Methods: Ethanol was administered by gavage as a 32% solution in water, and poly I:C was administered to activate NK cells. NK cell activity was measured using a standard 4 hr 51Cr release assay with YAC-1 tumor cells. The effects of corticosterone were evaluated by administration of a glucocorticoid antagonist (RU 486) or a dosage of corticosterone previously shown to induce similar blood levels as treatment with EtOH. Results: EtOH at 5-7 g/kg suppressed poly I:C-induced increases in NK cell lytic activity, and at least the lower end of this dosage range yields bloud EtOH levels that are relevant for humans (0.25-0.3%). This suppression was partially blocked in mice that were pretreated with a glucocorticoid antagonist, and administration of exogenous corticosterone also suppressed NK cell activation. Conclusions: EtOH-induced increases in corticosterone are apparently involved in the suppression of NK cell activation. This conclusion was supported by the lack of a direct effect of EtOH or its major metabolites (acetaldehyde and acetate) on NK cell activation by poly I:n vitro. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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