Ethanol Ingestion Inhibits Cell-Mediated Immune Responses of Unprimed T-Cell Receptor Transgenic Mice.

This paper introduces a transgenic ug) mouse in which the majority of the CWbearing T cells have T-cell receptors that react with ovalbumin (OVA) as a model for ethanol research. Although these Tg animals were bred onto the BALB/c genetic background, a strain generally considered to be nonpreferring in ethanol consumption, we determined that BALB/c mice would consume an ethanol-containing liquid diet, without significant mortality, and assessed alteration of specific immune responses. BALB/c, C57BU6 (B6), or (BALB/c x C57BL6)F1 hybrid (CB6F1) mice were fed LED containing 35,30,25, or 20% ethandaerived calories. Significant mortalii (>40%) was seen only in Wc and pronounced weight loss was seen in BALB/c, B6, CBEIFl mice when they were fed the diet containii the greatest ethanol concentration (LED35). Diets containing lesser amounts of ethanol did not cause mortalii. Liquid diets containing ≥30% ethand-derhred calories significantly impaired the chicken γ-globulbspecnic delayed hypersensitivity responses in Wc, B6, and CB6Flmice without significantly affecting the humoral immune response to sheep red Mood cells. We show that immunization of the Tg mice is not required for the development of a vigorous 'debyed hypersensitivity' response to OVA or the I-A'-restricted peptide OVL323-399 in mice fed standard solid lab chow or liquid control diet. In marked contrast, OVA Tg mice fed ethand show a profound inhibition of this immune response, indicating that ethand-induced inhibition of cell-mediated immunity occurs independently of antigen priming. [ABSTRACT FROM AUTHOR]