ArticleImmunity2012
Nitric oxide increases susceptibility of Toll-like receptor-activated macrophages to spreading Listeria monocytogenes.
Article in Immunity, 2012. 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 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
23 citing papers in PubMed, 46 citations in OpenAlex.
- Calpain-2 facilitates infection of the intracellular bacteria Listeria monocytogenes and invasion intestinal immune barrier by impairing nitric oxide homeostasis.Journal of advanced research · 2026Article
- Intestinal microbiome dysbiosis increaseseLife · 2024Article
- Local delivery of gaseous signaling molecules for orthopedic disease therapy.Journal of nanobiotechnology · 2023Review
- Strategies of Pathogens to Escape from NO-Based Host Defense.Antioxidants (Basel, Switzerland) · 2022Review
- Divergent Genetic Regulation of Nitric Oxide Production between C57BL/6J and Wild-Derived PWD/PhJ Mice Controls Postactivation Mitochondrial Metabolism, Cell Survival, and Bacterial Resistance in Dendritic Cells.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- The Opposing Role of Propionate in ModulatingFrontiers in microbiology · 2021Article
- Potential of oxygen and nitrogen reactive intermediates to disperse Listeria monocytogenes from biofilms.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2019Article
- RECON-Dependent Inflammation in Hepatocytes Enhances Listeria monocytogenes Cell-to-Cell Spread.mBio · 2018Article
- Gamma secretase dependent release of the CD44 cytoplasmic tail upregulates IFI16 in cd44-/- tumor cells, MEFs and macrophages.PloS one · 2018Article
- Listeria monocytogenes Has Both CytochromeInfection and immunity · 2017Article
- Article
- Type I IFN Inhibits Alternative Macrophage Activation during Mycobacterium tuberculosis Infection and Leads to Enhanced Protection in the Absence of IFN-γ Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- A dual-targeting approach to inhibit Brucella abortus replication in human cells.Scientific reports · 2016Article
- The Essential Role of Neutrophils during Infection with the Intracellular Bacterial Pathogen Listeria monocytogenes.Journal of immunology (Baltimore, Md. : 1950) · 2016Review
- An In Vivo Selection Identifies Listeria monocytogenes Genes Required to Sense the Intracellular Environment and Activate Virulence Factor Expression.PLoS pathogens · 2016Article
- Article
- Macrophages at the fork in the road to health or disease.Frontiers in immunology · 2015Article
- Article
- Regulation of NO synthesis, local inflammation, and innate immunity to pathogens by BET family proteins.Molecular and cellular biology · 2014Article
- Redox control of inflammation in macrophages.Antioxidants & redox signaling · 2013Review
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Toll-like receptor (TLR) stimulation activates macrophages to resist intracellular pathogens. Yet, the intracellular bacterium Listeria monocytogenes (Lm) causes lethal infections in spite of innate immune cell activation. Lm uses direct cell-cell spread to disseminate within its host. Here, we have shown that TLR-activated macrophages killed cell-free Lm but failed to prevent infection by spreading Lm. Instead, TLR signals increased the efficiency of Lm spread from "donor" to "recipient" macrophages. This enhancement required nitric oxide (NO) production by nitric oxide synthase-2 (NOS2). NO increased Lm escape from secondary vacuoles in recipient cells and delayed maturation of phagosomes containing membrane-like particles that mimic Lm-containing pseudopods. NO also promoted Lm spread during systemic in vivo infection, as shown by the fact that inhibition of NOS2 with 1400W reduced spread-dependent Lm burdens in mouse livers. These findings reveal a mechanism by which pathogens capable of cell-cell spread can avoid the consequences of innate immune cell activation by TLR stimuli.
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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.