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Pro-inflammatory cytokine treatments in primary mouse hepatocytes

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE96770 | GEO | 2017/10/10

SECONDARY ACCESSION(S): PRJNA379601

REPOSITORIES: GEO

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Pro-inflammatory cytokine treatments in primary mouse hepatocytes

Project description:Pro-inflammatory cytokine treatments in primary mouse hepatocytes

| PRJNA379601 | ENA

Characterization of gene expression changes following pro-inflammatory cytokine treatments in primary mouse hepatocytes

Project description:The cytokines interleukin 1β and 6 (IL-1β, IL-6) mediate the systemic acute and chronic inflammatory response. In liver, they both regulate the secretion of acute-phase proteins which curb infection and tissue damage. Using RNA-seq, we show that these cytokines regulate gene transcription in a multifaceted manner to modulate gene expression, leading both to synergistic and antagonistic expression patterns. By mapping changes in enhancer landscape and transcription factor occupancy following cytokine treatment, we show that synergistic gene expression was achieved by cooperation between cytokine-induced transcription factors on the chromatin template. At a subset of enhancers proximal to synergistically-induced acute-phase genes, IL-1β led to enhancer priming and an increase in STAT3 binding. These effects were mediated by NF-κB and were enhancer-specific rather that influencing the entirety of STAT3 binding. Our findings reveal that STAT3-NF-κB crosstalk at the chromatin template plays a major role in transcriptional regulation during inflammation

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Characterization of changes in enhancer activity and transcription factor binding following pro-inflammatory cytokine treatments in primary mouse hepatocytes

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Effects of Pro-Inflammatory Cytokines on Hepatic Metabolism in Primary Human Hepatocytes.

Project description:Three decades of hepatocyte transplantation have confirmed such a cell-based approach as an adjunct or alternative treatment to solid organ transplantation. Donor cell survival and engraftment were indirectly measured by hepatospecific secretive or released metabolites, such as ammonia metabolism in urea cycle defects. In cases of sepsis or viral infection, ammonia levels can significantly and abruptly increase in these recipients, erroneously implying rejection. Pro-inflammatory cytokines associated with viral or bacterial infections are known to affect many liver functions, including drug-metabolizing enzymes and hepatic transport activities. We examined the influence of pro-inflammatory cytokines in primary human hepatocytes, isolated from both normal donors or patients with metabolic liver diseases. Different measures of hepatocyte functions, including ammonia metabolism and phase 1-3 metabolism, were performed. All the hepatic functions were profoundly and significantly suppressed after exposure to concentrations of from 0.1 to 10 ng/mL of different inflammatory cytokines, alone and in combination. Our data indicate that, like phase I metabolism, suppression of phase II/III and ammonia metabolism occurs in hepatocytes exposed to pro-inflammatory cytokines in the absence of cell death. Such inflammatory events do not necessarily indicate a rejection response or loss of the cell graft, and these systemic inflammatory signals should be carefully considered when the immunosuppressant regiment is reduced or relieved in a hepatocyte transplantation recipient in response to such alleged rejection.

| S-EPMC9740548 | biostudies-literature

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