TLR4 showed a high expression in WT animals at 3 h and a significantly reduced expression in mFPR1 and mFPR2 TMPH hydrochloride deficient mice. On the other hand 6 h post LPS stimulation the TLR4 gene is significantly higher expressed in the mFPR1 and mFPR2-knockout mice. This leads to the conclusion that pathogen recognition might be delayed in the formyl peptide-receptor deficient mice and that both receptors contribute to this recognition and are essential for a stringent and correct procedure of this. This furthermore supports an immunomodulatory function of FPRs, which might not be exclusively provided by hematopoietic cells but also by parenchymal liver cells e.g. hepatocytes and hepatic stellate cells. In contrast to previous publications, the number of apoptotic cells in the liver of mFPR2-/- mice was the highest of all mice strains used in this study. The anti-apoptotic capabilities of FPR2/FPRL1 in primary human neutrophils are controversially discussed. Previous observations by Nagaoka et al. revealed that FPR2 is protective together with the P2X7 receptor. It was shown later that the distinct presence of Serum amyloid A, activates a protective signalling pathway which is P2X7 dependent, but FPR2/FPRL1 independent. So far, the participation of mFPR2 in the regulation of the liver inflammation remains to be investigated in detail. A better explanation for the higher rate of apoptosis is the TC-S 7006 stronger expression of the pro-inflammatory and pro-apoptotic cytokine TNF-a, a cytokine with pro-apoptotic abilities. It is significantly stronger expressed in either mFPR1-/- and mFPR2-/- mice in comparison to WT-mice. Furthermore these findings suggest a specific anti-apoptotic signalling of mFPR2 towards TNF-a induced pro-apoptotic signalling. Stimulation experiments using a combination of fMLF and pharmacological inhibitors for p38 and MEK resulted in reduced chemotaxis, adhesion and release of superoxide by neutrophils supporting a hypothesis of intracellular pathway modulation by FPRs. The investigation of liver proliferation to compensate the loss of liver mass, displayed an impairment of regenerative capacity in mFPR1 and mFPR2-deficient mice. Both genotypes showed a lower proliferation at 3 h and 6 h post LPS-induced liver injury, suggesting critical involvement of mFPR1 and mFPR2 in liver regeneration. Recent studies of liver regeneration showed that other member of the GPCR family especially the cannabinoid type 1 receptors support these findings.