For AST a slightly different pattern appears. Wild type mice had the highest levels of AST detectable in the serum compared to mFPR1 and mFPR2- deficient mice. 6 h post LPS the mFPR1 and mFPR2 knockout mice displayed significant higher levels of AST in the serum. These findings support a protective role for formyl peptide receptors during progression of LPS induced liver injury. The histological analysis after LPS-stimulation revealed a differential recruitment of immune cells in a time and genotype dependent manner. The cytokine IL-6 is not only known as a recruiting molecule for immune cells. It is described as one of the main drivers of hepatoprotection during liver injury, which mediates hepatoprotection against FAS-induced apoptosis as well as TNF-a induced apoptosis in the liver. The differential expression of IL-6, which is described as one of the most critical regulators of the immune response in the liver suggest, that mFPR1 mediated signalling is involved in the regulation of the early phase of inflammatory response in the liver and as a possible modulator of IL-6 signalling. A similar pattern is shown by the analysis of the expression of CXCL1 which correlates with the IL-6 expression. At the 6h time point increased migration of immune cells to the liver of mFPR1- and mFPR2-deficient mice. The more detailed analysis of those liver infiltrating cells was done by staining FFPE-liver tissues with antibodies for myeoloid cells or neutrophils. In comparison to wild type mice monocytes and neutrophils displayed a stronger presence in the livers of FPR1-/- and FPR2-/- mice 6 h after LPS stimulation. Interestingly mFPR2-/- mice showed a lower tendency regarding the number of Ly6G + – cells visible per view field. The closest explanation for this phenomenon is the link to the neutrophil recruiting cytokine CXCL1 which showed the same tendency at least on mRNA level at 3 h and at 6 h post LPS-stimulation. Differential roles for mFPR1 and mFPR2 regarding immune cell homing is not excluded for granulocytes and supported by the literature. It was shown recently, that FPR1 regulates the SB 223412 antiinflammatory response. Whether this response is correlated to the IL-6 signalling remains to be investigated. A further finding of the regulation of the anti-inflammatory response is visible for other PAMP-receptors such as TLR4 and TLR2. The analysis of SB 258585 hydrochloride theirs expression by qPCR reveals an increment in mFPR1 and mFPR2-deficient animals for TLR2 3 h and 6 h post LPS.