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Core immunometabolic reprogramming of Mycobacterium tuberculosis-infected mouse lungs and stage-specific effects by glutamine supplementation

GSE255689 Mus musculus (mouse) RNA-seq (gene expression) 24 samples Submitted 2026/02/10 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 24 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Samples
24 samples
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Summary (written by the submitters)
An emerging field of immunometabolism in tuberculosis (TB), an infectious disease caused by Mycobacterium tuberculosis, offers an opportunity for the development of urgently needed host-directed therapies (HDTs). Combining hypothesis-generating widely targeted metabolomics screening with transcriptome profiling in a mouse model of TB, we identify core metabolic programs and induction of signaling pathway mediated by mTORC1, the central regulator for cell metabolism, during immune cell activation.
Read the full summary ↓
In addition to expected enhanced glycolysis and arginine biosynthesis and catabolism, induction of glutaminolysis-associated pathways, as well as serine synthesis and its catabolism by mitochondrial branch of folate cycle underscores the pivotal role of amino acids and mitochondria metabolism in orchestrating host immunity against M. tuberculosis. A further test of the hypothesis reveals that glutamine supplementation of M. tuberculosis-infected mice not only reduces lung bacillary load, but also ameliorates progression of lung pathology. Pathway analysis of transcriptomic data further unveils infection stage-specific effects of glutamine on the immunometabolic response of immune cells. Glutamine bolsters host protective immunity during the chronic phase of infection by promoting core metabolic pathways, including glycolysis, while attenuating the overall host immune response during the acute phase. Collectively, the data emphasize the central role of amino acid and mitochondrial metabolism, in concert with other signaling and metabolic pathways, including glycolysis, in meeting the demand of activating immune cells for energy, signaling molecules, and anabolic precursors. These novel observations will provide therapeutic strategies for the development of novel HDTs for TB treatment by targeting specific metabolic pathways.
This dataset
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE255689_RAW.tar (it can run to tens of gigabytes).

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1076168 and SRA study SRP489592. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 24 more — browse all 24 samples with per-sample file links →

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