One of these secreted PAMPs is N-formylmethionyl-leucyl-phenylalanine peptide. The molecule fMLF is known as an inducer of chemotaxis for SBE 13 hydrochloride neutrophil granulocytes and monocytes after cellular damage. So far, two sources for fMLF are known. First, the bacterial cell wall could be identified as a source. Later the mitochondria were described as a second source for the secretion of fMLF. The release of fMLF is directly related to cellular apoptosis. Known receptors for the fMLF-peptide are the formyl peptide receptors. The FPRs belong to the family of G-protein coupled receptors. Up to now 3 members of the formyl-peptide receptor family are known. This family is an example for non-homology among receptor families. Sequence analysis of FPR1, FPR2 and FPR3 do show a similarity by 69% and 56%. Furthermore FPR1 shows high affinity towards fMLF, whereas FPR2 is a low-affinity receptor for fMLF and only high concentrations of fMLF are able to activate its signalling pathways. The third receptor FPR3 shows no affinity for fMLF at all. Also the distribution and the role of these receptors among tissues and cells are various. FPR1 is a relevant receptor for the chemotatic movement of neutrophils and monocytes. Neutrophils with a deficiency for FPR1 displayed an unorientated movement towards a side of injury and RWJ 50271 failed to reach this area. Besides its presence on the surface of hematopoietic cells FPR1 and FPR2, as well as theirs murine analogs, is also present on the surface of various organs. The second member of the FPR-Family, FPR2, also known as FPRL1/LipoxinA4-receptor is poorly chemotatic and only high concentrations of fMLF induce its signalling regarding to this PAMP. Furthermore the signalling of both receptors is highly various and depends on the receptor-ligand interaction. The role of bacterial translocation in liver diseases has changed in the last years. Being suggested as a late stage event, it was shown that early bacterial translocation is a main reason for the establishment of liver fibrosis and the progress of liver injury and survival of the bacterial infection was furthermore linked to the bacterial burden. These prior findings suggest a differential role of FPR in the recruitment of the different leucocyte subtypes and who might have different functions divided in between tissue resident and towards injury site recruited cells. Despite the fact of their well understood role in the chemotatic movement of hematopoietic cells, their role in parenchymal cells such as hepatocytes are poorly understood.