Evidence map›Paper›PMID 26989200›Full record

ArticleBlood2016

Peptidoglycan from the gut microbiota governs the lifespan of circulating phagocytes at homeostasis.

Christopher B Hergott, Aoife M Roche, Edwin Tamashiro, Thomas B Clarke, Aubrey G Bailey, Alice Laughlin, Frederic D Bushman, Jeffrey N Weiser

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
7.5field-weighted citation impact, top 2% of its field
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

70 citing papers in PubMed, 108 citations in OpenAlex.

  1. Review
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  12. Monocyte regulation by gut microbial signals.Trends in microbiology · 2023
    Review
  13. Article
  14. Microbiota-induced active translocation of peptidoglycan across the intestinal barrier dictates its within-host dissemination.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  15. Review
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  17. Reactive granulopoiesis depends on T-cell production of IL-17A and neutropenia-associated alteration of gut microbiota.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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  19. Review
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10 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 3 countries.

Christopher B HergottDepartment of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA;
Aoife M RocheDepartment of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA;
Edwin TamashiroDepartment of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA; Department of Ophthalmology, Otorhinolaryngology, and Head and Neck Surgery, Ribeirao Preto School of Medicine, University of São Paulo, São Paulo, Brazil;
Thomas B ClarkeMedical Research Council Centre for Molecular Bacteriology and Infection, Imperial College London, London, United Kingdom;
Aubrey G BaileyDepartment of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA;
Alice LaughlinDepartment of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA;
Frederic D BushmanDepartment of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA;
Jeffrey N WeiserDepartment of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA; Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA; and Department of Microbiology, New York University School of Medicine, New York, NY.
University of Pennsylvania · USImperial College London · GBNew York University · US

Funding

Virus & Reservoirs CoreP30AI045008 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI Ronald G Collman · 1999 to 2026
$78.6M
ROLE OF OPACITY VARIATION IN PNEUMOCOCCAL PATHOGENESISR01AI038446 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEISER, JEFFREY NEAL · 1996 to 2019
$7.4M
Mechanisms of Pneumococcal Persistence During CarriageR37AI038446 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Jeffrey Neal Weiser · 2020 to 2026
$3.8M
Lung Transplant Microbiome and Chronic Allograft DysfunctionR01HL113252 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI BUSHMAN, FREDERIC D, CHRISTIE, JASON D · 2013 to 2016
$2.9M
Early Events in Pneumococcal ColonizationR01AI105168 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEISER, JEFFREY NEAL · 2014 to 2018
$2.1M
Training in bacteriologyT32AI060516 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI GOULIAN, MARK D, ZHU, JUN · 2006 to 2015
$2.0M
Medical Research Council MR/J006874/1NHLBI NIH HHS R01 HL113252NIAID NIH HHS P30 AI045008NIAID NIH HHS R01 AI038446NIAID NIH HHS R01 AI105168NIAID NIH HHS R37 AI038446NIAID NIH HHS T32 AI060516Wellcome Trust 107660
6 · The paper itself

Abstract

Maintenance of myeloid cell homeostasis requires continuous turnover of phagocytes from the bloodstream, yet whether environmental signals influence phagocyte longevity in the absence of inflammation remains unknown. Here, we show that the gut microbiota regulates the steady-state cellular lifespan of neutrophils and inflammatory monocytes, the 2 most abundant circulating myeloid cells and key contributors to inflammatory responses. Treatment of mice with broad-spectrum antibiotics, or with the gut-restricted aminoglycoside neomycin alone, accelerated phagocyte turnover and increased the rates of their spontaneous apoptosis. Metagenomic analyses revealed that neomycin altered the abundance of intestinal bacteria bearing γ-d-glutamyl-meso-diaminopimelic acid, a ligand for the intracellular peptidoglycan sensor Nod1. Accordingly, signaling through Nod1 was both necessary and sufficient to mediate the stimulatory influence of the flora on myeloid cell longevity. Stimulation of Nod1 signaling increased the frequency of lymphocytes in the murine intestine producing the proinflammatory cytokine interleukin 17A (IL-17A), and liberation of IL-17A was required for transmission of Nod1-dependent signals to circulating phagocytes. Together, these results define a mechanism through which intestinal microbes govern a central component of myeloid homeostasis and suggest perturbations of commensal communities can influence steady-state regulation of cell fate.

Indexed as

HomeostasisAdoptive TransferAnimalsAnimals, CongenicAnti-Bacterial AgentsApoptosisCell SurvivalDiaminopimelic AcidFemaleGastrointestinal MicrobiomeGerm-Free LifeInterleukin-17MiceMice, Inbred C57BLMice, KnockoutMonocytesAnti-Bacterial AgentsDiaminopimelic AcidIl17a protein, mouseInterleukin-17N(2)-(gamma-D-glutamyl)-meso-2,2'-diaminopimelic acidNod1 protein, mouseNod1 Signaling Adaptor ProteinNod2 protein, mouseNod2 Signaling Adaptor ProteinPeptidoglycanTlr2 protein, mouseTlr4 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID26989200
PMCPMC4874226
OpenAlexW2412773516

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.