Evidence map›Paper›PMID 39511195›Full record

ArticleNature communications2024

Altered genomic methylation promotes Staphylococcus aureus persistence in hospital environment.

Yuriko Yamazaki, Tomoka Ito, Seitaro Nakagawa, Takashi Sugihira, Chinami Kurita-Tachibana, Amer E Villaruz, Kensuke Ishiguro, Barbora Salcman, Shuo Li, Sanami Takada and 26 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Dysbiosis in the Pathogenesis of Atopic Dermatitis.The Journal of dermatology · 2026
    Review
  8. Article
  9. Review
  10. Biofilm-associated genes inFrontiers in microbiology · 2026
    Review
  11. Alternative and Synergistic Strategies Against Antibiotic-ResistantInternational journal of microbiology · 2026
    Review
  12. Article
  13. Review
  14. Article
  15. The Role of Skin Dysbiosis and Quorum Sensing in Atopic Dermatitis.JID innovations : skin science from molecules to population health · 2025
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

36 authors.

Yuriko Yamazaki *Department of Dermatology, Chiba University Graduate School of Medicine, 260-8670, Chiba, Japan.ORCID 0000-0002-4026-8306
Tomoka Ito *Department of Dermatology, Osaka University Graduate School of Medicine, 565-0871, Osaka, Japan.ORCID 0009-0001-7281-6928
Seitaro Nakagawa *Department of Dermatology, Chiba University Graduate School of Medicine, 260-8670, Chiba, Japan.
Takashi SugihiraDepartment of Dermatology, Osaka University Graduate School of Medicine, 565-0871, Osaka, Japan.
Chinami Kurita-TachibanaCutaneous Allergy and Host Defense, Immunology Frontier Research Center, Osaka University, 565-0871, Osaka, Japan.
Amer E VillaruzPathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 20852, Bethesda, USA.
Kensuke IshiguroDepartment of Chemistry and Biotechnology, Graduate School of Engineering, The University of Tokyo, 113-8656, Tokyo, Japan.ORCID 0000-0001-6651-1960
Barbora SalcmanCutaneous Allergy and Host Defense, Immunology Frontier Research Center, Osaka University, 565-0871, Osaka, Japan.
Shuo LiCutaneous Allergy and Host Defense, Immunology Frontier Research Center, Osaka University, 565-0871, Osaka, Japan.
Sanami TakadaDepartment of Dermatology, Chiba University Graduate School of Medicine, 260-8670, Chiba, Japan.
Naohiro InoharaDepartment of Pathology and Rogel Cancer Center, University of Michigan Medical School, MI, 48109, Ann Arbor, USA.
Yoko KusuyaMedical Mycology Research Center, Chiba University, 260-8673, Chiba, Japan.ORCID 0000-0002-5724-487X
Aki ShibataDepartment of Infection Control Science, Graduate School of Pharmaceutical Sciences, Chiba University, 260-8675, Chiba, Japan.
Masakazu TamaiDepartment of Dermatology, Osaka University Graduate School of Medicine, 565-0871, Osaka, Japan.
Reika AoyamaDepartment of Dermatology, Osaka University Graduate School of Medicine, 565-0871, Osaka, Japan.
Kanako InoueResearch Center for Ultra-High Voltage Electron Microscopy, Osaka University, 567-0047, Osaka, Japan.
Shota MurataDivision of Clinical Laboratory, Chiba University Hospital, 260-8677, Chiba, Japan.
Kazuyuki MatsushitaDivision of Clinical Laboratory, Chiba University Hospital, 260-8677, Chiba, Japan.ORCID 0000-0001-6742-0761
Akiko MiyabeDivision of Clinical Laboratory, Chiba University Hospital, 260-8677, Chiba, Japan.
Toshibumi TaniguchiDivision of Infection Control, Chiba University Hospital, 260-8677, Chiba, Japan.ORCID 0000-0002-7732-9870
Hidetoshi IgariDivision of Infection Control, Chiba University Hospital, 260-8677, Chiba, Japan.ORCID 0000-0001-7754-3458
Naruhiko IshiwadaDepartment of Infectious Diseases, Medical Mycology Research Center, Chiba University, 260-8673, Chiba, Japan.ORCID 0000-0002-7508-1330
Masateru TaniguchiDepartment of Bio-Nanotechnology, The Institute of Scientific and Industrial Research, Osaka University, 565-0871, Osaka, Japan.ORCID 0000-0002-0338-8755
Taka-Aki NakadaDepartment of Emergency and Critical Care Medicine, Chiba University Graduate School of Medicine, 260-8670, Chiba, Japan.
Hiroyuki MatsueDepartment of Dermatology, Chiba University Graduate School of Medicine, 260-8670, Chiba, Japan.
Manabu FujimotoDepartment of Dermatology, Osaka University Graduate School of Medicine, 565-0871, Osaka, Japan.ORCID 0000-0002-3062-4872
Haruka HishikiDepartment of Pediatrics, Chiba University Graduate School of Medicine, 260-8670, Chiba, Japan.
Yoshiteru OsoneDepartment of Pediatrics, Chiba University Graduate School of Medicine, 260-8670, Chiba, Japan.ORCID 0000-0001-5712-7019
Hiromichi HamadaDepartment of Pediatrics, Chiba University Graduate School of Medicine, 260-8670, Chiba, Japan.
Naoki ShimojoDepartment of Pediatrics, Chiba University Graduate School of Medicine, 260-8670, Chiba, Japan.ORCID 0000-0002-8076-0493
Tsutomu SuzukiDepartment of Chemistry and Biotechnology, Graduate School of Engineering, The University of Tokyo, 113-8656, Tokyo, Japan.ORCID 0000-0002-9731-1731
Michael OttoPathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 20852, Bethesda, USA.ORCID 0000-0002-2222-4115
Gabriel NúñezDepartment of Pathology and Rogel Cancer Center, University of Michigan Medical School, MI, 48109, Ann Arbor, USA.ORCID 0000-0002-6529-2695
Hiroki TakahashiMedical Mycology Research Center, Chiba University, 260-8673, Chiba, Japan.ORCID 0000-0001-5627-1035
Akiko TakayaMedical Mycology Research Center, Chiba University, 260-8673, Chiba, Japan.ORCID 0000-0003-1726-7150
Yuumi NakamuraCutaneous Allergy and Host Defense, Immunology Frontier Research Center, Osaka University, 565-0871, Osaka, Japan. ymatsuoka@derma.med.osaka-u.ac.jp.ORCID 0000-0001-6256-8302

Funding

Staphylococcal pathogenesisZIAAI000904 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI OTTO, MICHAEL · 2009 to 2025
$22.6M
Division of Intramural Research, National Institute of Allergy and Infectious Diseases (Division of Intramural Research of the NIAID) ZIA-AI000904Intramural NIH HHS ZIA AI000904Japan Agency for Medical Research and Development (AMED) 18gm6010016h0002Japan Agency for Medical Research and Development (AMED) 23gm1610004h0003
6 · The paper itself

Abstract

Staphylococcus aureus can cause outbreaks and becomes multi-drug resistant through gene mutations and acquiring resistance genes. However, why S. aureus easily adapts to hospital environments, promoting resistance and recurrent infections, remains unknown. Here we show that a specific S. aureus lineage evolved from a clone that expresses the accessory gene regulator (Agr) system to subclones that reversibly suppressed Agr and caused an outbreak in the hospital setting. S. aureus with flexible Agr regulation shows increased ability to acquire antibiotic-resistant plasmids, escape host immunity, and colonize mice. Bacteria with flexible Agr regulation shows altered cytosine genomic methylation, including the decreased 5mC methylation in transcriptional regulator genes (pcrA and rpsD), compared to strains with normal Agr expression patterns. In this work, we discover how altered genomic methylation promotes flexible Agr regulation which is associated with persistent pathogen colonization in the hospital environment.

Indexed as

Bacterial ProteinsDNA MethylationGene Expression Regulation, BacterialStaphylococcal InfectionsStaphylococcus aureusTrans-ActivatorsAnimalsFemaleGenome, BacterialHospitalsHumansMiceAgr protein, Staphylococcus aureusBacterial ProteinsTrans-Activators

Identifiers

PMID39511195
PMCPMC11544029

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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.