ArticleCell2014
An extracellular bacterial pathogen modulates host metabolism to regulate its own sensing and proliferation.
Article in Cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 88 citations in OpenAlex.
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- Shining a light on bacterial environmental cue integration and its relation to metabolism.Molecular microbiology · 2023Article
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- Streptococcus pyogenes TrxSR Two-Component System Regulates Biofilm Production in Acidic Environments.Infection and immunity · 2021Article
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- Reprogramming of microRNA expression via E2F1 downregulation promotes Salmonella infection both in infected and bystander cells.Nature communications · 2021Article
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Corrections and comments
- Commented on by
- Erratum issuedChen, Catherine Youting [corrected to Cheng, Catherine Youting]
Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Successful infection depends on the ability of the pathogen to gain nutrients from the host. The extracellular pathogenic bacterium group A Streptococcus (GAS) causes a vast array of human diseases. By using the quorum-sensing sil system as a reporter, we found that, during adherence to host cells, GAS delivers streptolysin toxins, creating endoplasmic reticulum stress. This, in turn, increases asparagine (ASN) synthetase expression and the production of ASN. The released ASN is sensed by the bacteria, altering the expression of ∼17% of GAS genes of which about one-third are dependent on the two-component system TrxSR. The expression of the streptolysin toxins is strongly upregulated, whereas genes linked to proliferation are downregulated in ASN absence. Asparaginase, a widely used chemotherapeutic agent, arrests GAS growth in human blood and blocks GAS proliferation in a mouse model of human bacteremia. These results delineate a pathogenic pathway and propose a therapeutic strategy against GAS infections.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.