Inhibition of TLR8- and TLR4-induced Type I IFN induction by alcohol is different from its effects on inflammatory cytokine production in monocytes

Maoyin Pang, Shashi Bala, Karen Kodys, Donna Catalano, Gyongyi Szabo

Prolonged alcohol consumption is a significant co-factor in the progression of chronic viral infections including hepatitis C and HIV, which are both single-stranded RNA viruses. Toll like receptor 8 （TLR8）, a pattern recognition receptor expressed in monocytes, senses viral single stranded RNA as a danger signal and leads to the induction of Type I interferon （IFN） as well as the pro-inflammatory cytokine, tumor necrosis factor alpha （TNF alpha）. Lipopolysaccharide （LPS）, a Toll like receptor 4 （TLR4） ligand, was shown to affect inflammatory cell activation after alcohol consumption and in HIV and HCV infections. Here we hypothesized that alcohol exposure modulates TLR8- and TLR4-ligand-induced monocyte activation and affects both type I IFN and inflammatory cytokine induction.