ArticleNature microbiology2016
A quorum-sensing signal promotes host tolerance training through HDAC1-mediated epigenetic reprogramming.
Article in Nature microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- Pooled it
- Pseudomonas aeruginosa-derived volatile organic compounds modulate AhR signaling to dysregulate airway mucus homeostasis.Nature communications · 2026Article
- The gut microbiota shapes the human and murine breath volatilome.Cell metabolism · 2026Article
- Reprogramming host histone modifications by bacterial pathogens.Molecules and cells · 2026Review
- RNA modifications shape innate immunity and cellular adaptation during bacterial respiratory infection.Frontiers in immunology · 2026Review
- Effects ofFrontiers in microbiology · 2026Article
- Trained immunity in the lung.eLife · 2025Review
- Deficiency of HMGN2 enhances antibacterial activity of macrophages by promoting H3 histone modification-mediated CD14/iNOS expression.Frontiers in immunology · 2025Article
- Revealing the impact ofFrontiers in immunology · 2025Article
- Review
- Article
- Article
- Unveiling the modulation ofFrontiers in microbiology · 2024Article
- Mechanisms of the Quorum Sensing Systems ofCurrent medicinal chemistry · 2024Review
- Pulmonary Pathogen-Induced Epigenetic Modifications.Epigenomes · 2023Review
- Article
- Modulation of innate immunity in airway epithelium for host-directed therapy.Frontiers in immunology · 2023Review
- High-expression of the innate-immune related gene UNC93B1 predicts inferior outcomes in acute myeloid leukemia.Frontiers in genetics · 2023Article
- Tackling recalcitrant Pseudomonas aeruginosa infections in critical illness via anti-virulence monotherapy.Nature communications · 2022Article
- Human M1 macrophages express unique innate immune response genes after mycobacterial infection to defend against tuberculosis.Communications biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The mechanisms by which pathogens evade elimination without affecting host fitness are not well understood. For the pathogen Pseudomonas aeruginosa, this evasion appears to be triggered by excretion of the quorum-sensing molecule 2-aminoacetophenone, which dampens host immune responses and modulates host metabolism, thereby enabling the bacteria to persist at a high burden level. Here, we examined how 2-aminoacetophenone trains host tissues to become tolerant to a high bacterial burden, without compromising host fitness. We found that 2-aminoacetophenone regulates histone deacetylase 1 expression and activity, resulting in hypo-acetylation of lysine 18 of histone H3 at pro-inflammatory cytokine loci. Specifically, 2-aminoacetophenone induced reprogramming of immune cells occurs via alterations in histone acetylation of immune cytokines in vivo and in vitro. This host epigenetic reprograming, which was maintained for up to 7 days, dampened host responses to subsequent exposure to 2-aminoacetophenone or other unrelated pathogen-associated molecules. The process was found to involve a distinct molecular mechanism of host chromatin regulation. Inhibition of histone deacetylase 1 prevented the immunomodulatory effects of 2-aminoacetophenone. These observations provide the first mechanistic example of a quorum-sensing molecule regulating a host epigenome to enable tolerance of infection. These insights have enormous potential for developing preventive treatments against bacterial infections.
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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.