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Transcriptome profiling of the hepatic acute-phase response in LPS-treated dHepaRG cells.

ABSTRACT: HepaRG cells are a human hepatic cell line that upon differentiation (dHepaRG) provide many features of primary hepatocytes, including high metabolic activity, detoxification, bile acid and urea synthesis. They are also able to undergo the acute-phase response upon inflammatory stimulation - the massive upregulation of serum proteins which support the systemic immune response. The aim of this study was to investigate the transcriptomic reprogramming of dHepaRG cells upon Lipopolysaccharide (LPS) treatment. LPS potently activates immune responses in dHepaRG cells by inducing autocrine IL6-signalling and the expression of acute-phase genes. However, it is known that homeostatic liver functions are downregulated consecutively. The RNA-Seq data should deliver an overview about affected pathways and factors which are involved in this reprogramming process.

ORGANISM(S): Homo sapiens

PROVIDER: GSE230325 | GEO | 2024/03/01

REPOSITORIES: GEO

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Project description:Vaccination reduces morbidity and mortality from pneumonia but its effect on the tissue-level response to infection is still poorly understood. We evaluated pneumonia disease progression, acute phase response and lung gene expression profiles in mice inoculated intranasally with virulent gram-positive Streptococcus pneumoniae serotype (ST) 3, with and without prior immunization with pneumococcal polysaccharide ST 3 (PPS3), or co-immunization with PPS3 and with a low dose of lipopolysaccharide (LPS). Pneumonia severity was assessed in the acute phase, 5, 12, 24 and 48 h post-inoculation (p.i.) and the resolution phase of 7 days p.i. Primary PPS3 specific antibody production was upregulated and IgM binding to pneumococci increased in PPS3-immunized mice. Immunizations with PPS3 or PPS3 + LPS decreased bacterial recovery the lung and blood at 24 and 48 h and increased survival. Microarray analysis of whole lung RNA revealed significant changes in the acute phase protein serum amyloid A (SAA) between noninfected and infected mice, which were attenuated by immunization. SAA transcripts were higher in the liver and lungs of infected controls, and SAA protein was elevated in serum, but decreased in PPS3-immunized mice. Thus, during a virulent pneumonia infection, prior immunization with PPS3 in an IgM-dependent manner as well as co-immunization with PPS3 + LPS attenuated pneumonia severity and promoted resolution of infection, concomitant with significant regulation of cytokine gene expression in the lungs, and acute phase proteins in the lungs, liver and serum. Each lung RNA sample represented an individual mouse, creating biological repeats for each treatment. In-vivo treatments were as follows: non-infected lung (vehicle-immunized) control (n=5), infected lung (vehicle-immunized) control at 48 hr post-inoculation (n=5), PPS3 and LPS co-immunized lung at 48 hr post-inoculation (n=4) and PPS3 and LPS co-immunized lung at 7 days post-inoculation (n=4).

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Transcriptome profiling of the hepatic acute-phase response in LPS-treated dHepaRG cells.

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