LPS hypersensitivity of gp130 mutant mice is independent of elevated hematopoietic TLR4 signaling. Mus musculus

The inflammatory mediator IL6 induced by LPS, which signals via TLR4, has been shown to feedback and augment TLR4 signaling when over-produced in LPS hypersensitive gp130F/F mice. The identity of the LPS/TLR4 responsive inflammatory signaling pathways and gene networks which are modulated by IL6 are unknown. Therefore, to understand the molecular consequences of gp130 hyperactivity in non-haemopoietic tissue on LPS-induced systemic inflammation, global gene expression profiling of livers was performed. Overall design: The mouse 22K compugen oligo array from the Adelaide Microarray Facility was used to investigate the effect of LPS treatment on the livers of wildtype and gp130F/F mutant mice. Livers of both wildtype mice and gp130F/F mice at 6hr post LPS injection and also control livers wer collected. Each experimental group had 3 independant mice. In total 12 arrays were performed with a total of three biological replicates. A common reference design was used for this experiment. RNA extracted from eight pooled 17.5dpc C57BL/6 mouse embryos was used as the reference sample. 6 wildytpe mice and 6 gp130F/F mice were used in this study, with 3 mice of each genotype treated with LPS.