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Methylglyoxal activates the NRF2 pathway and impairs immune responses controlling the growth control of Mycobacterium tuberculosis (Mtb) in macrophages.

GSE271061 Mus musculus Expression profiling by high throughput sequencing 9 samples Submitted 2024/07/20 Platform GPL13112
Summary
We compared the transcriptome profile of M. tuberculosis-infected murine bone marrow derived macrophages (BMM) treated or not with 200 uM methylglyoxal (MGO) and uninfected controls as described below. We found 3606 differentially expressed genes (DEGs) between uninfected and M. tuberculosis-infected BMM, being approximately half of these upregulated . 1699 DEGs were determined by comparing Mtb-MGO vs M. tuberculosis BMM, with 2/3 of these DEGs downregulated. Genes in the glyoxalate, glutathione and selenocompound metabolic KEEG pathways were increased comparing Mtb-MGO vs M. tuberculosis BMM. Instead genes involved in type I IFN responses, cytokine receptor and chemokine signalling gene ontology clusters (GO) were increased after infection with Mtb as compared to uninfected controls and decreased in Mtb-MGO vs M. tuberculosis BMM.
Published in
The inhibition of TXNRD1 by methylglyoxal impairs the intracellular control of Mycobacterium tuberculosis
Li H, Liu R, Kathamuthu GR et al. · Redox biology 2025 · PMID 40602278 · doi:10.1016/j.redox.2025.103741
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Also filed as BioProject PRJNA1129523 and SRA study SRP516826. Searching any of these in the dataset finder brings you back here.

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