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Endothelial cell-derived oxysterol ablation attenuates experimental autoimmune encephalomyelitis

ABSTRACT: Endothelial cell-derived oxysterol ablation attenuates experimental autoimmune encephalomyelitis

PROVIDER: PRJNA899025 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22214611.fastq.gz	Fastqsanger.gz
	SRR22214612.fastq.gz	Fastqsanger.gz
	SRR22214613.fastq.gz	Fastqsanger.gz
	SRR22214614.fastq.gz	Fastqsanger.gz
	SRR22214615.fastq.gz	Fastqsanger.gz

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Endothelial cell-derived oxysterol ablation attenuates experimental autoimmune encephalomyelitis

Project description:The vasculature is a key regulator of leukocyte trafficking into the central nervous system (CNS) during inflammatory diseases including multiple sclerosis. However, the impact of endothelial-derived factors on other aspects of CNS immune responses remains unknown. Bioactive lipids, in particular oxysterols downstream Cholesterol-25-hydroxylase (Ch25h) promote neuroinflammation but their functions in the CNS remain unclear. Using a floxed-reporter Ch25h knock-in mice, we traced Ch25h expression to CNS endothelial cells (ECs) and myeloid cells and demonstrated that Ch25h-specific ablation in ECs attenuates experimental autoimmune encephalomyelitis. Mechanistically, inflamed Ch25h-deficient CNS ECs displayed altered lipid metabolism favoring polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) expansion relative to other leukocyte subsets that suppress encephalitogenic T lymphocytes proliferation. Finally, endothelial Ch25h-deficiency combined with mobilization of immature neutrophils into circulation resulted in nearly complete EAE protection. Our findings reveal a central role for CNS endothelial-derived Ch25h in promoting neuroinflammation by regulating expansion of immunosuppressive myeloid cell populations.

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Endothelial cell-derived oxysterol ablation attenuates experimental autoimmune encephalomyelitis

Project description:The vasculature is a key regulator of leukocyte trafficking into the central nervous system (CNS) during inflammatory diseases including multiple sclerosis (MS). However, the impact of endothelial-derived factors on CNS immune responses remains unknown. Bioactive lipids, in particular oxysterols downstream of Cholesterol-25-hydroxylase (Ch25h), promote neuroinflammation but their functions in the CNS are not well understood. Using floxed-reporter Ch25h knock-in mice, we trace Ch25h expression to CNS endothelial cells (ECs) and myeloid cells and demonstrate that Ch25h ablation specifically from ECs attenuates experimental autoimmune encephalomyelitis (EAE). Mechanistically, inflamed Ch25h-deficient CNS ECs display altered lipid metabolism favoring polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC) expansion, which suppresses encephalitogenic T lymphocyte proliferation. Additionally, endothelial Ch25h-deficiency combined with immature neutrophil mobilization into the blood circulation nearly completely protects mice from EAE. Our findings reveal a central role for CNS endothelial Ch25h in promoting neuroinflammation by inhibiting the expansion of immunosuppressive myeloid cell populations.

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Project description:The ubiquitin ligase Peli1 has previously been suggested as a potential treatment target in multiple sclerosis since the knock-out induced less activated microglia and less inflammation in the CNS of experimental autoimmune encephalomyelitis in mice. In the present study the brain proteomes of Peli1 knock-out mice and wild-type mice were analyzed and compared before disease induction and after 10 and 20 days of experimental autoimmune encephalomyelitis using quantitative proteomics. The brain samples were analyzed using TMT labeling of small pools of samples and verified using label-free of individual mice.

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