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Staphylococcus aureus infection-driven myeloid-derived suppressor cells

ABSTRACT: Critical role of immune metabolism in Staphylococcus aureus infection-driven myeloid-derived suppressor cells and disease tolerance

PROVIDER: PRJEB37074 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3978860.fastq.gz	Fastqsanger.gz
	ERR3978891.fastq.gz	Fastqsanger.gz
	ERR3979014.fastq.gz	Fastqsanger.gz
	ERR3975185.fastq.gz	Fastqsanger.gz
	ERR3978695.fastq.gz	Fastqsanger.gz

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Immune metabolism regulates myeloid-derived suppressor cells expansion and disease tolerance in Staphylococcus aureus chronic infection

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LKB1 is a suppressor of amino acid-driven gluconeogenesis in the liver

Project description:Excessive hepatic glucose production is a major contributor to the hyperglycemia observed in Type 2 diabetes mellitus. It is widely accepted that it is due to an increase in hepatic gluconeogenesis. While much attention has been devoted to the transcriptional regulation of key gluconeogenic enzymes, much less is known about the regulation of amino acid catabolism that provides gluconeogenic substrates. Here, we emphasize a novel role of LKB1 in this regulation. We show that mice with a hepatocyte-specific deletion of Lkb1 have increased hepatic amino acid catabolism for gluconeogenesis. This occurred during fasting, as well as during the postprandial period, identifying Lkb1 as a critical suppressor of hepatic postprandial gluconeogenesis. Hepatic Lkb1 deletion was also associated with severe alterations in whole body metabolism leading to decreased lean body mass deposition on MRI analysis and, at a longer term, cachexia and sarcopenia as a consequence of the diversion of amino acids for liver metabolism at the expense of muscle. Using genetic and pharmacological approaches, we identified the aminotransferases and Agxt and as critical effectors of the suppressor function of Lkb1 in amino acid-driven gluconeogenesis.

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RNASeq analysis of Myeloid Derived Suppressor Cells (MDSCs) from MC38 syngeneic mice to study their role on tumour intrinsic pathways (STING/IFN) for driving ceralasertib (AZD6738) efficacy

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