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A number of studies have shown that consumption of alcohol inhibits immune function in both adult humans and animals (Jerrells et al. 1986). In adults, ethanol is immunosuppressive, decreasing both the cellularity of the thymus and spleen and interfering directly with B and T-lymphocyte responses. Additionally, alcohol suppresses the phagocytic activity of macrophages and reduces NK cell activity (Seelig et al. 1996). Ethanol consumption alters cytokine production, including IL-2, IL-5, IL-6, IL-10, and reduces the capacity of T cells to use IL-2. TNF-a production was impaired as was the distribution of TNF-a receptor on alveolar macrophages (Seelig et al. 1996).

Alcohol readily crosses the placenta and has a well-documented effect on the developing fetus. Maternal alcohol consumption can cause altered development ranging from a mild reduction in birth weight to severe manifestations of fetal alcohol syndrome (FAS). FAS is a multifaceted disorder characterized by growth deficits, CNS dysfunction, mental retardation, and cranial facial deformities. In addition, these children have defects in host defense and consequently an increase in the number and severity of infections (Johnson et al. 1981; Steinhausen et al. 1982; Moscatello et al. 1999). Some children with FAS have been shown to have long-

lasting deficits in both humoral and cell-mediated immunity including lymphopenia, eosinophilia, decreased lymphocyte mitogenesis, lower IgG levels, and can suffer increased illness such as pneumonia and meningitis during the first few years of life (Johnson et al. 1981; Giberson and Weinberg 1997).

Experimental animals exposed to prenatal alcohol exhibit suppressed immune function. Specifically, animals exposed during development to alcohol displayed decreased lymphocyte response to the mitogens con A and LPS, reduced serum IgM and IgG levels, reduced specific antibody production to T-dependent antigen, suppressed IL-2 and TNF production, and reduced immune transfer resulting in decreased passive immune protection for the neonate (Adkins et al. 1987; Monjan and Mandell 1980; Ewald and Frost 1987; Wolcott et al. 1995; Seelig et al. 1996, 1999). This indicates prenatal ethanol exposure affects specific B- and T cell function as well as cytokine production in ethanol-exposed pups (Seelig et al. 1996). Many of these immunological deficits are long-lasting, including a reduced number of thymocytes, a reduced proliferative response of B- and T-lymphocytes to mitogens, reduced splenic and thymic T-lymphoblast response to IL-2, and deficits in CMI including graft vs. host response and contact hypersensitivity (Wolcott et al. 1995; Giberson and Weinberg 1997; Moscatello et al. 1999).

The suppression of immune function with prenatal alcohol exposure can be exacerbated by additional lactational exposure. Seelig et al. (1996) exposed the following four groups of mice to ethanol: 1.) dams fed ethanol during pregnancy and lactation and pups fed ethanol after weaning, 2.) dams received ethanol through pregnancy and lactation, 3.) dams received ethanol through delivery, and 4.) dams received ethanol only through lactation. Ethanol was passed from dam to pup in all four groups, and all pups had some degree of suppressed neonatal immunity. The greatest immunologic suppression was seen in pups receiving both prenatal and postnatal exposure. In a later study, mice exposed to maternal ethanol during pregnancy and lactation and who also consumed alcohol into adulthood demonstrated additional reductions in total Tand B-cells numbers, as well as specific IgM and IgG antibodies. The sequential reduction in cell numbers and antibody levels from unexposed mice, to first-generation ethanol animals (dams), to offspring exposed to ethanol prenatally and also through adulthood, suggests that there is a cumulative effect of in utero ethanol exposure and subsequent alcohol consumption (Seelig et al. 1999).

Fetal mice exposed to alcohol in utero have reduced thymic cellularity (Wolcott et al. 1995) resulting in thymic atrophy (Ewald and Frost 1987). Reduction in thymocytes in mice exposed to ethanol during fetal life may be due to altered development of T-lymphocyte populations resulting in thymic hypocellularity. Recent work using fetal thymus organ culture has shown that alcohol-exposed fetuses have decreased numbers of double positive CD4+ CD8+ T cells and increased number of single positive cells as well as increased apoptosis compared to control fetuses (Giberson and Weinberg 1997). The decrease of double positive CD4+ CD8+ T cells has also been seen in mouse fetuses in vivo. Because both T-helper and T-cytotoxic cells arise from this population of thymocytes with a decrease in double positive cells, one would expect reduced numbers of these mature T-lymphocytes.

B cell development is also affected by prenatal alcohol exposure. Mice exposed to ethanol in utero had decreased numbers of pre-B cells in the bone marrow and decreased numbers of total B cells in the spleen and bone marrow (Moscatello et al. 1999). In this study, the rate at which both mature and immature B cells accumulated in the spleen was reduced in prenatally ethanol-exposed animals. Immature and mature B cells did not reach control levels until 4 weeks of age in prenatally exposed animals. The pool of precursor B cells did not reach control levels by 5 weeks, the last point measured. It was hypothesized that the pool of B-lineage progenitors is specifically affected by the prenatal alcohol exposure (Moscatello et al. 1999).

Male offspring tend to be affected more than female offspring by in utero alcohol exposure (Giberson and Weinberg 1995, 1997). The sex differences and specific immune defects become more pronounced with stress. This indicates that the impaired immune system has some ability to compensate for the deficits resulting from prenatal ethanol exposure and may not demonstrate immune suppression when tested under nonstressed conditions. When rat pups, particularly males, were challenged by a stressor, the deficits in immune function became more apparent (Giberson and Weinberg 1995, 1997).

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