For liver, a network was constructed that features cytochrome monooxygenases, glutathione transferases and circadian genes (PER1, 2) together with a number of transcription factors (Creb, NFkB, DBP, AP1, NFE2) as hub genes. This network was based on the CI treatment but many of the genes are also changed by Chronic, DID and LPS treatments. For all differentially expressed genes, there was significant overlap among all alcohol treatments and for LPS with all alcohol groups. This demonstrates that although some of the changes in the liver transcriptome may be due to the metabolism of large amounts of ethanol in this tissue, many of the effects are mimicked by LPS, which suggests that a component of alcohol action on liver is due to immune activation. This is consistent with the key role of inflammation in alcoholic liver disease [24], [25].
