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RNAseq analysis of bone marrow plasma cells from KD-treated mice

ABSTRACT: Humoral immunological memory is essential for the protection against pathogens post primary infection or vaccination. This protection relies on the long-term survival of pathogen-specific memory B cells and lone-lived plasma cells. We found that ketogenic diet (KD) impairs the humoral immunological memory by depleting the plasma cells. We performed functional analysis of these bone marrow plasma cells from control mice or KD-treated mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE262108 | GEO | 2026/01/27

REPOSITORIES: GEO

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RNAseq analysis of bone marrow plasma cells from fasted mice

Project description:Humoral immunological memory is essential for the protection against pathogens post primary infection or vaccination. This protection relies on the long-term survival of pathogen-specific memory B cells and lone-lived plasma cells. We found that fasting impairs the humoral immunological memory by depleting the plasma cells. We performed functional analysis of these bone marrow plasma cells from Ad Lib mice or fasted mice.

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Transcription profiling of rat brain hippocampi of animals fed the ketogenic diet (KD) to provide insight into the anticonvulsant action of KD

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Mus musculus strain:C57BL/6J

Project description:Fasting impairs humoral immunological memory

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Transcription profiling of mouse livers from animals fed a ketogenic diet (KD), a diet high in fat and low in carbohydrates

Project description:Analysis of liver gene transcription during feeding of a ketogenic diet. Ketogenic diets may alter physiologic and metabolic profiles in a direction that favors weight loss. C57BL/6J mice were maintained for six weeks on either chow or ketogenic diet. Mice eating KD had lower weights, 90% reduction in insulin levels and increased energy expenditure compared to animals fed chow. Despite consumption of a very high fat diet serum lipids remained normal. Here we show that consumption of KD shifted liver metabolism to drastically increased fatty acid oxidation. Concurrently, expression of genes involved in fatty acid synthesis were markedly suppressed. Reference: A high fat, ketogenic diet induces a unique metabolic state in mice. Kennedy AR, Pissios P, Out H, Xue B, Asakura K, Furukawa N, Marino FE, Liu FF, Kahn BB, Liberman TA, Maratos-Flier E. in press, 2007, Am J Physiol Metab 292. Experiment Overall Design: Eight week old C57BL/6 mice were fed either chow (Labdiet 5008, Pharmserv) or KD (F3666, Bio-Serv) for six weeks. Livers were harvested in the morning in ad lib fed animals. Total RNA from 2-3 animals in each group was used for Affymetrix analysis.

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Gene expression of wild-type and Nix-/-Bnip3-/- memory B cells

Project description:Memory B cells are long-lived lymphocytes essential for humoral immunological memory. Autophagy is required for the long-term survival of memory B cells, however, the molecular mechanisms for the protection by autophagy have not been fully elucidated. Here we show that mitochondrial autophagy mediated by Nix and Bnip3 prevents necroptosis in memory B cells by maintaining mitochondrial homeostasis and normal lipid metabolism. In mice with B cell-specific deletion of Nix and Bnip3, memory B cells showed significant increases in viable mitochondria and de novo fatty acid synthesis, with accumulation of lipid droplets in the cytoplasm and accelerated cell death. Inhibiting the mitochondrial citrate transporter Slc25a1 or silencing the necroptosis gene Ripk3 rescued Nix–/–Bnip3–/– memory B cells in vivo. These data indicate that Nix- and Bnip3-dependent mitochondrial autophagy in memory B cells is important for restricting de novo fatty acid synthesis and preventing necroptosis. Our results suggest a mechanism for autophagy in the maintenance of mitochondrial homeostasis for the protection of immunological memory.

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Impact of Ketogenic diet on aging associated gene expression in the brain.

Project description:The Ketogenic Diet (KD) was shown to extend lifespan and preserve memory in aged mice. We carried out RNA-seq on brains of mice aged 13-26 months on standard Carbohydrate-rich control Diet (CD) vs KD, to better understand KD's mechanism for memory preservation.

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Gene expression changes in ketogenic and high-fat diets

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Project description:Sepsis patients suffer from severe metabolic and immunologic dysfunction that may be amplified by standard nutritional approaches relying primarily on carbohydrates. We here hypothesize that a ketogenic diet improves sepsis treatment. We conducted a monocentric open-labeled randomized controlled trial enrolling 40 adult sepsis patients. Patients were randomly assigned to either ketogenic diet (KD) or standard high-carbohydrate nutrition for 14 days and followed up until day 30. The primary outcome measure was β-hydroxybutyrate (BHB) serum concentration on day 14. We assessed feasibility and safety of KD, as well as diet-associated clinical and immunological changes. The respective nutrition protocols were successfully applied, dropouts did not occur. Regression analysis revealed a greater increase in BHB concentrations from baseline to day 14 in KD patients compared to controls. Metabolic side effects were not observed under ketogenic diet. Ventilation-free, vasopressor-free, dialysis-free and ICU-free days significantly increased in patients under ketogenic diet. Transcriptome profiling of both CD4+ and CD8+ T cells at day 14 revealed substantial differential regulation of gene expression in the KD vs. the control group indicating a reduced T-cell activation and a shift towards a more regulated immunity.

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Ketogenic diet therapy for pediatric epilepsy is associated with alterations in the human gut microbiome that confer seizure resistance in mice

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