ArticleThe Journal of clinical investigation2019
Bacterial sepsis triggers an antiviral response that causes translation shutdown.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 61 citations in OpenAlex.
- The redundant protein synthesis gene Aimp1 challenges the canonical inverse relationship between translation and autophagy.Communications biology · 2026Article
- Hyaluronan 35 prevents endotoxin-mediated dysregulated skeletal muscle proteostasis during ethanol exposure.American journal of physiology. Endocrinology and metabolism · 2026Article
- Roles of the integrated stress response in regulation of inflammatory reactions.Frontiers in immunology · 2026Review
- A kappa opioid receptor agonist, difelikefalin, improves acute kidney injury in experimental sepsis models.PloS one · 2026Article
- Molecular Mechanisms of Sepsis-Associated Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Review
- Glutamate utilization fuels rapid production of mitochondrial ROS in dendritic cells and drives systemic inflammation during tularemia.Science advances · 2025Article
- Comparison of sepsis-associated acute kidney injury with different degrees and causes reveals patterns in mitochondrial metabolism and immune infiltration changes.Scientific reports · 2025Article
- Acute inflammation induced by the Escherichia coli lipopolysaccharide considerably increases the systemic and brain exposure of olanzapine after oral administration in mice.The international journal of neuropsychopharmacology · 2025Article
- miRNA and mRNA Signatures in Human Acute Kidney Injury Tissue.The American journal of pathology · 2025Article
- Article
- Inflammation primes the murine kidney for recovery by activating AZIN1 adenosine-to-inosine editing.The Journal of clinical investigation · 2024Article
- RNA-Seq of an LPS-Induced Inflammation Model Reveals Transcriptional Profile Patterns of Inflammatory Processes.Life (Basel, Switzerland) · 2024Article
- tRNA-Derived Small RNAs: A Novel Regulatory Small Noncoding RNA in Renal Diseases.Kidney diseases (Basel, Switzerland) · 2024Article
- Development of novel liver-targeting glucocorticoid prodrugs.Medicine in drug discovery · 2024Article
- Screening of prognostic core genes based on cell-cell interaction in the peripheral blood of patients with sepsis.Open life sciences · 2024Article
- Article
- Peptide derived from SLAMF1 prevents TLR4-mediated inflammation in vitro and in vivo.Life science alliance · 2023Article
- Dimension-agnostic and granularity-based spatially variable gene identification using BSP.Nature communications · 2023Article
- Inflammation primes the kidney for recovery by activating AZIN1 A-to-I editing.bioRxiv : the preprint server for biology · 2023Article
- Multi-biological functions of intermedin in diseases.Frontiers in physiology · 2023Review
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8 authors at 2 institutions in 1 country.
Funding
Abstract
In response to viral pathogens, the host upregulates antiviral genes that suppress translation of viral mRNAs. However, induction of such antiviral responses may not be exclusive to viruses, as the pathways lie at the intersection of broad inflammatory networks that can also be induced by bacterial pathogens. Using a model of Gram-negative sepsis, we show that propagation of kidney damage initiated by a bacterial origin ultimately involves antiviral responses that result in host translation shutdown. We determined that activation of the eukaryotic translation initiation factor 2-α kinase 2/eukaryotic translation initiation factor 2α (Eif2ak2/Eif2α) axis is the key mediator of translation initiation block in late-phase sepsis. Reversal of this axis mitigated kidney injury. Furthermore, temporal profiling of the kidney translatome revealed that multiple genes involved in formation of the initiation complex were translationally altered during bacterial sepsis. Collectively, our findings imply that translation shutdown is indifferent to the specific initiating pathogen and is an important determinant of tissue injury in sepsis.
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