Evidence map›Paper›PMID 34637779›Full record

ArticleCell host & microbe2021

Episymbiotic Saccharibacteria suppresses gingival inflammation and bone loss in mice through host bacterial modulation.

Otari Chipashvili, Daniel R Utter, Joseph K Bedree, Yansong Ma, Fabian Schulte, Gabrielle Mascarin, Yasmin Alayyoubi, Deepak Chouhan, Markus Hardt, Felicitas Bidlack and 4 more

Open access · greenAbstract read
In one paragraph

Article in Cell host & microbe, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
11.7field-weighted citation impact, top 1% 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

76 citing papers in PubMed, 110 citations in OpenAlex.

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  4. A host-encoded prophage targets a Candidate Phyla Radiation bacterium and shapes episymbiotic interactions.Proceedings of the National Academy of Sciences of the United States of America · 2026
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16 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

14 authors at 4 institutions in 1 country.

Otari ChipashviliThe Forsyth Institute, Cambridge, MA 02142, USA.
Daniel R UtterDivision of Geological and Planetary Sciences, California Institute of Technology, Pasadena, CA 91125, USA.
Joseph K BedreeThe Forsyth Institute, Cambridge, MA 02142, USA; Section of Oral Biology, Division of Oral Biology and Medicine, School of Dentistry, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Yansong MaThe Forsyth Institute, Cambridge, MA 02142, USA.
Fabian SchulteThe Forsyth Institute, Cambridge, MA 02142, USA; Department of Developmental Biology, Harvard School of Dental Medicine, Boston, MA 02115, USA.
Gabrielle MascarinThe Forsyth Institute, Cambridge, MA 02142, USA.
Yasmin AlayyoubiThe Forsyth Institute, Cambridge, MA 02142, USA.
Deepak ChouhanThe Forsyth Institute, Cambridge, MA 02142, USA; Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA 02115, USA.
Markus HardtThe Forsyth Institute, Cambridge, MA 02142, USA; Department of Developmental Biology, Harvard School of Dental Medicine, Boston, MA 02115, USA.
Felicitas BidlackThe Forsyth Institute, Cambridge, MA 02142, USA; Department of Developmental Biology, Harvard School of Dental Medicine, Boston, MA 02115, USA.
Hatice HasturkThe Forsyth Institute, Cambridge, MA 02142, USA.
Xuesong HeThe Forsyth Institute, Cambridge, MA 02142, USA; Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA 02115, USA.
Jeffrey S McLeanDepartment of Periodontics, University of Washington, Seattle, WA 98119, USA; Department of Microbiology, University of Washington, Seattle, WA 98195, USA.
Batbileg BorThe Forsyth Institute, Cambridge, MA 02142, USA; Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA 02115, USA. Electronic address: bbor@forsyth.org.
Harvard University · USCalifornia Institute of Technology · USUniversity of California, Los Angeles · USUniversity of Washington · US

Funding

Domestication and characterization of TM7-the most elusive oral phylumR01DE023810 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Xuesong He, Jeffrey Scott McLean · 2014 to 2026
$6.6M
Making a quantum leap in plaque research with modern sciencesR01DE020102 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HE, XUESONG, MCLEAN, JEFFREY SCOTT · 2010 to 2020
$3.7M
Impact of Saccharibacteria and their bacterial hosts in Periodontal and Inflammatory DiseasesR01DE031274 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI Batbileg Bor · 2022 to 2026
$2.5M
Studying the Protective Effects of Normal Oral FloraR01DE026186 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HE, XUESONG, MCLEAN, JEFFREY SCOTT · 2016 to 2020
$2.1M
Moving Beyond Diversity by Revealing Biological Functions of Uncultured BacteriaR01GM095373 · NIGMS · J. CRAIG VENTER INSTITUTE, INC. · PI MCLEAN, JEFFREY SCOTT, YOOSEPH, SHIBU · 2011 to 2014
$1.7M
Molecular and pathogenic study of an oral TM7 strain, the first cultivated ultra-small bacteriumR00DE027719 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI BOR, BATBILEG · 2020 to 2022
$747k
Systematic approach to explore the microbial interactomeR21DE027199 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUX, RENATE, MCLEAN, JEFFREY SCOTT · 2017 to 2018
$441k
Molecular and pathogenic study of an oral TM7 strain, the first cultivated ultra-small bacteriumK99DE027719 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI BOR, BATBILEG · 2018 to 2019
$268k
Shedding Light on Microbial Dark MatterF31DE026057 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BEDREE, JOSEPH KERNAN · 2016 to 2020
$156k
NIDCR NIH HHS F31 DE026057NIDCR NIH HHS K99 DE027719NIDCR NIH HHS R00 DE027719NIDCR NIH HHS R01 DE020102NIDCR NIH HHS R01 DE023810NIDCR NIH HHS R01 DE026186NIDCR NIH HHS R01 DE031274NIGMS NIH HHS R01 GM095373
6 · The paper itself

Abstract

Saccharibacteria (TM7) are obligate epibionts living on the surface of their host bacteria and are strongly correlated with dysbiotic microbiomes during periodontitis and other inflammatory diseases, suggesting they are putative pathogens. However, due to the recalcitrance of TM7 cultivation, causal research to investigate their role in inflammatory diseases is lacking. Here, we isolated multiple TM7 species on their host bacteria from periodontitis patients. These TM7 species reduce inflammation and consequential bone loss by modulating host bacterial pathogenicity in a mouse ligature-induced periodontitis model. Two host bacterial functions involved in collagen binding and utilization of eukaryotic sialic acid are required for inducing bone loss and are altered by TM7 association. This TM7-mediated downregulation of host bacterial pathogenicity is shown for multiple TM7/host bacteria pairs, suggesting that, in contrast to their suspected pathogenic role, TM7 could protect mammalian hosts from inflammatory damage induced by their host bacteria.

Indexed as

Bacterial Physiological PhenomenaSymbiosisActinobacteriaActinomycesAlveolar Bone LossAnimalsBacteriaBacterial InfectionsCollagenDental PlaqueDown-RegulationGenes, BacterialGingivitisHumansMaleMiceCollagenN-Acetylneuraminic AcidActinobacteriaActinomycesbacterial symbiosiscandidate phyla radiationhuman microbiomehuman oral microbiomeinflammatory diseaseperiodontitisSaccharibacteriaTM7

Identifiers

PMID34637779
PMCPMC8595704
OpenAlexW3206371077

What OpenQuestion holds

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Registered trials

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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.