Chronic alcohol consumption regulates the expression of poly immunoglobulin receptor (pIgR) and secretory IgA in the gut

- Chronic alcohol (EtOH) alters monocytes and dendritic cells ratios in the gut.
- EtOH decreases the number of T cells synthesizing IFN-γ in Peyer's patches.
- EtOH decreases IgA and pIgR levels in small (SI) and large (LI) intestine feces.
- EtOH decreases pIgR levels in SI homogenates.
- EtOH favors the appearance of an inflammatory cytokine profile in SI homogenates.

The effect of ethanol (EtOH) on the gut immune system was analyzed using an experimental model previously described, where EtOH was provided ad libitum in the drinking water in a 20% w/v concentration for up to 12 weeks. Dendritic cells, T cells and macrophages were analyzed in Peyer's patches and the small intestines using flow cytometry. Cytokine and immunoglobulin levels were analyzed in sera, feces, and homogenates from small and large intestines and lungs. Decreases in the proportion of T cells and alterations in dendritic cells and macrophages were observed after EtOH treatment. Levels of immunoglobulin A (IgA) increased in tissue homogenates but decreased in small intestine fecal contents. Meanwhile poly-immunoglobulin receptor (pIgR) levels decreased in tissue homogenates and fecal contents. Levels of cytokines associated with the regulation of pIgR expression decreased for IL-10 and TGF-β, and increased for IFN-γ and IL-17 in the small intestine. The data indicate that chronic EtOH consumption disrupts the homeostasis of the mucosal immune system by altering the phenotype and functionality of multiple immune cell types, leading to a diminished secretion of SIgA, due to pIgR expression decreased.