ArticleInfection and immunity2012
Hyperinduction of host beta interferon by a Listeria monocytogenes strain naturally overexpressing the multidrug efflux pump MdrT.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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.
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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.
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Who cites it
42 citing papers in PubMed, 66 citations in OpenAlex.
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
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- Cyclic di-AMP, a multifaceted regulator of central metabolism and osmolyte homeostasis inmicroLife · 2023Review
- Transmembrane Protein LMxysn_Microorganisms · 2022Article
- Virulence gene repression promotesGut microbes · 2020Article
- Pathogenic Biohacking: Induction, Modulation and Subversion of Host Transcriptional Responses byToxins · 2020Review
- Why is Listeria monocytogenes such a potent inducer of CD8+ T-cells?Cellular microbiology · 2020Review
- New Insights on the Role of the pLMST6 Plasmid inFrontiers in microbiology · 2019Article
- Cyclic Dimeric Guanosine Monophosphate: Activation and Inhibition of Innate Immune Response.Journal of innate immunity · 2019Review
- Antimicrobial Resistance inMicrobiology spectrum · 2018Review
- RECON-Dependent Inflammation in Hepatocytes Enhances Listeria monocytogenes Cell-to-Cell Spread.mBio · 2018Article
- Article
- Amplifying IFN-γ Signaling in Dendritic Cells by CD11c-Specific Loss of SOCS1 Increases Innate Immunity to Infection while Decreasing Adaptive Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- The Emerging Roles of STING in Bacterial Infections.Trends in microbiology · 2017Review
- Article
- Getting "Inside" Type I IFNs: Type I IFNs in Intracellular Bacterial Infections.Journal of immunology research · 2017Review
- Group B Streptococcus Degrades Cyclic-di-AMP to Modulate STING-Dependent Type I Interferon Production.Cell host & microbe · 2016Article
- Type I IFN Does Not Promote Susceptibility to Foodborne Listeria monocytogenes.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Nuclease-Resistant c-di-AMP Derivatives That Differentially Recognize RNA and Protein Receptors.Biochemistry · 2016Article
- [Cloning, expression, and purification of c-di-AMP metabolism-related genes from Porphyromonas gingivalis].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Many pathogens regulate or modify their immune-stimulating ligands to avoid detection by their infected hosts. Listeria monocytogenes, a facultative intracellular bacterial pathogen, interacts with multiple components of mammalian innate immunity during its infection cycle. During replication within the cytosol of infected cells, L. monocytogenes utilizes two multidrug efflux pumps, MdrM and MdrT, to secrete the small nucleic acid second messenger cyclic-di-AMP (c-di-AMP). Host recognition of c-di-AMP triggers the production of type I interferons, including beta interferon (IFN-β), which, surprisingly, promote L. monocytogenes virulence. In this study, we have examined the capacity of multiple laboratory and clinical isolates of L. monocytogenes to stimulate host production of IFN-β. We have identified the L. monocytogenes strain LO28 as able to hyperinduce IFN-β production in infected cells ∼30-fold more than the common laboratory clone L. monocytogenes strain 10403S. Genomic analyses determined that LO28 contains a naturally occurring loss-of-function allele of the transcriptional regulator BrtA and correspondingly derepresses expression of MdrT. Surprisingly, while derepression of MdrT resulted in hyperstimulation of IFN-β, it results in significant attenuation in multiple mouse models of infection. While type I interferons may promote L. monocytogenes virulence, this study demonstrates that unregulated expression of the c-di-AMP-secreting efflux pump MdrT significantly restricts virulence in vivo by an unknown mechanism.
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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.