Chronic ethanol exposure affects in vivo migration of hepatic dendritic cells to secondary lymphoid tissue.

The mechanisms by which chronic ethanol (EtOH) consumption results in an immune-compromised state have not been fully elucidated. No studies to date have ascertained whether EtOH affects the migratory capacity of dendritic cells (DC), potent immune regulators. We hypothesized that EtOH exposure might affect hepatic and splenic DC trafficking to secondary lymphoid tissues and the resulting immune response. Hepatic DC from EtOH-treated animals migrated in greater numbers to draining lymphoid tissue than controls, whereas spleen DC were unaffected. Moreover, hepatic EtOH-exposed (E) DC induced more vigorous priming of allogeneic T cells in vivo compared with splenic EDC or controls. Altered hepatic EDC migration was independent of either CCR7 or CD11a expression, with no striking changes in surface expression of other adhesion molecules analyzed. The modified trafficking to secondary lymphoid tissue observed for hepatic EDC may play a role in the altered immune response to microbial pathogens in chronic alcohol users.