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, C57BL6 (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 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 greater than or equal to 30% ethanol-derived calories significantly impaired the chicken gamma-globulin-specific delayed hypersensitivity responses in BALB/c, B6, and CB6F/mice without significantly affecting the humoral immune response to sheep red blood cells. We show Bat immunization of the Tg mice 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 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.