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K. pneumoniae induced metabolic stress promotes immunotolerance [single-cel RNA-seq]

ABSTRACT: K. pneumoniae induced metabolic stress promotes immunotolerance [single-cel RNA-seq]

PROVIDER: PRJNA786553 | ENA |

REPOSITORIES: ENA

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K. pneumoniae induced metabolic stress promotes immunotolerance

Project description:K. pneumoniae induced metabolic stress promotes immunotolerance

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K. pneumoniae induced metabolic stress promotes immunotolerance [single-cel RNA-seq]

Project description:Metabolites generated in response to infection have a major role in shaping the nature of the immune response. We predicted that the metabolic response to the highly prevalent Klebsiella pneumoniae sequence type 258 (Kp ST258) strains is responsible for their ability to persist in the lungs, despite the expected proinflammatory signaling evoked by LPS. By combining in situ metabolic imaging and comprehensive transcriptional analyses, we demonstrate that Kp ST258 activates host glutaminolysis and fatty acid oxidation (FAO), generating an oxidant-rich microenvironment predisposed to the accumulation of anti-inflammatory monocyte populations. In a setting not unlike that generated by some tumors, metabolically active Kp ST258 elicits an immunotolerant, instead of a proinflammatory response. The bacteria in turn adapt to airway oxidants by upregulation of the Type VI Secretion System (T6SS), which is highly conserved across these strains worldwide. The global success of Kp ST258 can be explained, to a major extent, by their metabolic activity that promotes a permissive immune response to which the bacteria adapt.

2022-08-09 | GSE190262 | GEO

K. pneumoniae induced metabolic stress promotes immunotolerance

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Klebsiella pneumoniae-induced metabolic stress promotes immunotolerance

Project description:The metabolic stress associated with K. pneumoniae ST258 infection promotes immunosuppression and drives bacterial adaptation.

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Shear stress promotes metabolic changes in endothelial cells

Project description:Here we investigated how shear stress influences the metabolic behavior of endothelial cells (ECs) using a combination of transcriptomics, tracer metabolomics. Transcriptomics analysis of ECs under wall shear stress (WSS) showed an increase in the glutamine, asparagine, alanine, aspartate, and glutamate biochemical activity while the downregulated gene signature suggested a reduction of the glycolysis activity. Metabolomics analysis of the medium from static and WSS cultured ECs revealed that -upon WSS- changes in the nutritional preferences of ECs occurred. Using tracer metabolomics, we further evidenced that WSS promotes glutamine anaplerosis into the Krebs cycle and a decrease in the glycolytic metabolism of ECs in vitro. In conclusion, our findings elucidate the nutritional preferences of ECs and reveal the importance of a physical stimulus (WSS) in the regulation of EC metabolism in vitro.

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