Epigenetic mechanisms contribute to enhanced expression of immune response genes in the liver of cows after experimentally induced Escherichia coli mastitis.

Endotoxins, such as lipopolysaccharide (LPS), are released during infection with Gram-negative bacteria, which can result in excessive activation of toll-like receptor (TLR) signalling. The aim of the present study was to investigate whether epigenetic mechanisms are involved in controlling the onset and progression of the systemic inflammatory response. Using chromatin accessibility by real-time (CHART) PCR to assess livers from cows with experimentally induced Escherichia coli mastitis, this study demonstrated that the chromatin at the site of the promoters of the genes encoding TLR2, TLR4, lipopolysaccharide binding protein (LBP) and haptoglobin (HP) was opened up 24 h after infection, accompanied by enhanced mRNA expression by these genes. Such modulation did not occur in the same samples for the αS1-casein promoter, which served as a negative control. Demethylation of the TLR4 promoter accompanied opening up of chromatin. These data suggest that modulation of epigenetic factors might offer a novel approach to treating adverse systemic reactions elicited in cows with E. coli mastitis.