Background and aims Ethanol has been elaborated to have a beneficial effect on destructive arthritis. Nevertheless, the effect of ethanol on the development of systemic lupus erythematosus (SLE) remains controversial. This study was performed to determine the potential role of moderate ethanol consumption in SLE pathological progression and clarify its functional mechanism.
Methods We used MRL/lpr mice to assess whether ethanol drinking has any impact on the development of SLE and investigated whether ethanol regulates pathologic progression of SLE through inhibiting lipid rafts.
Results We found that 10% ethanol in vivo delayed disease progression and organ damage and prolonged survival. In vitro ethanol treatment not only inhibited the aggregation, proliferation, adhesion molecule expression and IFN-γ secretion of T cells, but also decreased lipid raft clustering on T cells. In addition, ethanol inhibited SLE serum-induced skin inflammation and monocyte differentiation into dendritic cells (DCs). Furthermore, ethanol treatment of monocytes that were in the process of differentiating into DCs decreased lipid raft clustering.
Conclusions These data strongly support the viewpoint that ethanol delays the disease progression of SLE by inhibiting lipid raft clustering and suggest that moderate drinking of ethanol may have a protective value for patients with SLE.
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