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)F1 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 mica 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 ≤30% ethanol-derived calories significantly impaired the chicken γ-globulin-specific delayed hypersensitivity responses in BALB/c, B6, and CB6F1 mice without significantly affecting the humoral immune response to sheep red blood cells. We show that immunization of the Tg mica is not required for the development of a vigorous 'delayed hypersensitivity' response to OVA or the I-A(d)-restricted peptide OVA_323-399 in mice fed standard solid lab chow or liquid control diet. In marked contrast, OVA Tg mica fed ethanol show a profound inhibition of this immune response, indicating that ethanol-induced inhibition of cell-mediated immunity occurs independently of antigen priming.