Abstract
Ethanol (alcohol) consumption can modify immune responses. Moderate ethanol use is associated with lower production of mediators of inflammation and has anti-inflammatory effect, while ethanol abuse and alcoholism are linked with augmentation of inflammatory responses. Ethanol exposure can result in functional alterations of macrophages and other cells of the innate immune system. These cells recognize microbial antigens through Toll-like receptors (TLRs). Molecular mechanisms underlying the inflammatory responses stimulated via TLRs involve activation of intracellular signaling pathways that include mitogen-activated protein kinases (MAPKs) and transcription factor NFκB. Growing evidence indicates that ethanol can affect these cellular events in a manner that depends on the organ or cell type and the pattern of ethanol administration (moderate or acute versus chronic).
Keywords: Ethanol, inflammation, cardiovascular disease, cytokines, toll-like receptors, MAPK
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