Ethanol ingestion inhibits cell-mediated immune responses of unprimed T-cell receptor transgenic mice.

This paper introduces a transgenic (Tg) mouse in which the majority of the CD4-bearing 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, C57BL/6 (B6), or (BALB/c x C57BL/6)F-1 hybrid (CB6F1) mice were fed LED containing 35, 30, 25, or 20% ethanol-derived calories. Significant mortality (> 40%) was seen only in BALB/c and pronounced weight loss was seen in BALB/c, B6, CB6F1 mice when they were fed the diet containing the greatest ethanol concentration (LED35). Diets containing lesser amounts of ethanol did not cause mortality. Liquid diets containing > or = 30% ethanol-derived calories significantly impaired the chicken gamma-globulin-specific delayed hypersensitivity responses in BALB/c, B6, and CB6F1mice without significantly affecting the humoral immune response to sheep red blood cells. We show that immunization of the Tg mice is not required for the development of a vigorous "delayed hypersensitivity" response to OVA or the I-Ad-restricted peptide OVA323-339 in mice fed standard solid lab chow or liquid control diet. In marked contrast, OVA Tg mice fed ethanol show a profound inhibition of this immune response, indicating that ethanol-induced inhibition of cell-mediated immunity occurs independently of antigen priming.