Regulation von Peroxiredoxinen in aktivierten und infizierten murinen Makrophagen Macrophages play a decisive role during inflammation as well as for the activation of defense mechanisms against bacterial infections. In response to inflammatory cytokines and bacterial products macrophages generate nitric oxide (NO) and reactive oxygen species (ROS) that not only transduce redox sensitive signalling but also induce cell damage. Amongst others the ubiquitously expressed peroxiredoxins (Prxs) are important components of the cellular defense system. They constitute a family of six thiol dependent peroxidases which are able to reduce hydrogen peroxide organic peroxides and reactive nitrogen compounds. Next to their antioxidant capacity peroxiredoxins are involved in the regulation of cell proliferation signal transduction as well as apoptosis. This thesis investigated the constitutive expression of peroxiredoxins in bone marrow derived macrophages (BMM) of C57BL 6 and BALB c mice and the alteration of the gene expression of Prxs by treatment with interferon  (IFN) and lipopolysaccharide (LPS). While in C57BL 6 BMM the mRNA induction of Prx 1 2 4 and 6 was dependent on the inducible NO synthase (iNOS) only the LPS and IFN increased gene expression of Prx 1 and Prx 6 was mediated by iNOS derived NO. Moreover the influence of tyrosine kinase JAK2 and Src family tyrosine kinases phosphatidylinositol 3 kinase (PI3K) and protein kinase C as well as p44 42 MAPK p38 MAPK and c Jun NH2 terminal kinase (JNK) on the enhanced gene expression of Prx 1 5 und 6 was analysed after stimulation with LPS and IFN. For the first time it could be shown that gene expression of Prx 6 is inducible by several Nrf2 (nuclear factor erythroid 2p45 (NF E2) related factor 2 ) activators and LPS and IFN induced Prx 6 mRNA expression is partially mediated by Nrf2 in primary macrophages. In addition the cytosolic phospholipase A2 (cPLA2) was involved in the regulation of the LPS and IFN induced transcription of Prx 5 and Prx 6 ... Makrophage Burkholderia Immunreaktion Interferon <gamma > Stickstoffmonoxid Synthase NADPH Oxidase Signaltransduktion MAP Kinase Peroxiredoxin antioxidative Enzyme Wirt Pathogen Interaktion Lipopolysaccharid Cytokine peroxiredoxin intracellular signalling Burkholderia macrophage cyclooxygenase