In Table 2, up- and downregulation were calculated from real time data, genes were clustered according to the mode used for Table 1. Table 2 TaqMan? Custom Array microfluidic card system was used to assess expression status at the mRNA level of 18 selected genes (see Table 1) in reference to 5 reference selleck chem inhibitor genes (Gapdh, Est1, Rlp3, Mdh-1, Rpl37). When comparing microarray and microfluidic card system, they exhibited a high level of congruency (Spearman correlation rho=0.81, p=7.87e-5). Overview of differential gene regulation Most (34 from 36, 94%) of upregulated genes were annotated to processes, while 2 genes (6%) were annotated to of hepatocytes.

Upregulated genes associated with (n=34) could be clustered into functional subgroups including (n=15), (n=6), (n=10), (n=2) and (n=1). Two downregulated genes related to and , respectively (Tab. 1). The genes (n=35) either associated with an or an pathway, are schematically drawn in (Fig. 1). Figure 1 Schematic hepatic cell type interaction profile linked to differentially expressed genes. In the following paragraph, first upregulated, then downregulated genes will be presented more in details: Immune response/defense [M?]; up-regulated “type”:”entrez-nucleotide”,”attrs”:”text”:”BC023105″,”term_id”:”18605634″,”term_text”:”BC023105″BC023105, Tgtp, Gvin1 These belong to the interferon-inducible p47 GTPases.

Interferons (with a preference IFN-�� over ��/��) bind to their respective receptors. For Tgtp, the binding is followed by phosphorylation of STAT1 and rapid translocation of P-STAT1 dimers to the nucleus. There, the complex activates transcription of p47 GTPases by binding to the IFN-�� activation site (GAS) in the promoter. The gene products enable Brefeldin_A the M? phagosome to be part of the innate defense of cells to infection, but its role in such defense has not yet been clearly defined [6]. GBPs (GBP1, GBP2, 5830443L24Rik, GBP8) GBPs are upregulated in macrophages in response to IFN-��. GBP-1 is a large GTPase that is induced by inflammatory cytokines and acts antiangiogenically through the inhibition of endothelial cell proliferation and migration [7]. Interestingly, some GBPs are upregulated in mice infected with intracellular pathogens such as L. monocytogenes and T. gondii and are colocalized with T. gondii in infected cells [8].