Evidence map›Paper›PMID 19933833›Full record

ArticleInfection and immunity2010

Transitions in oral and intestinal microflora composition and innate immune receptor-dependent stimulation during mouse development.

Mizuho Hasegawa, Toshifumi Osaka, Kazuki Tawaratsumida, Takashi Yamazaki, Hiroyuki Tada, Grace Y Chen, Satoshi Tsuneda, Gabriel Núñez, Naohiro Inohara

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

42 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Effects of Milk Replacer-BasedMicrobiology spectrum · 2022
    Article
  8. Article
  9. A Mouse Periodontitis Model With Humanized Oral Bacterial Community.Frontiers in cellular and infection microbiology · 2022
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Neonatal acquisition ofScience (New York, N.Y.) · 2017
    Article
  19. Article
  20. Observational
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

9 authors at 2 institutions in 2 countries.

Mizuho HasegawaDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Toshifumi Osaka
Kazuki Tawaratsumida
Takashi Yamazaki
Hiroyuki Tada
Grace Y Chen
Satoshi Tsuneda
Gabriel Núñez
Naohiro Inohara
University of Michigan–Ann Arbor · USWaseda University · JP

Funding

Nod2: A Susceptibility Gene for Crohn's DiseaseR01DK061707 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NUNEZ, GABRIEL · 2002 to 2017
$4.7M
Regulation of Oral Bacteria by Pattern Recognition ReceptorsR01DE018503 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI INOHARA, NAOHIRO · 2008 to 2012
$1.8M
NIDCR NIH HHS R01 DE018503NIDCR NIH HHS R01DE018503NIDDK NIH HHS R01 DK061707NIDDK NIH HHS R01 DK61707
6 · The paper itself

Abstract

Commensal bacteria possess immunostimulatory activities that can modulate host responses to affect development and homeostasis in the intestine. However, how different populations of resident bacteria stimulate the immune system remains largely unknown. We characterized here the ability of intestinal and oral microflora to stimulate individual pattern recognition receptors (PRRs) in bone marrow-derived macrophages and mesothelial cells. The intestinal but not oral microflora elicited age- and cell type-specific immunostimulation. The immunostimulatory activity of the intestinal microflora varied among individual mice but was largely mediated via Toll-like receptor 4 (TLR4) during breast-feeding, whereas it became TLR4 independent after weaning. This transition was associated with a change from a microflora rich in TLR4-stimulatory proteobacteria to one dominated by Bacteroidales and/or Clostridiales that poorly stimulate TLR4. The major stimulatory activity of the intestinal microflora was still intact in NOD1-, NOD2-, TLR2-, TLR4-, TLR5-, TLR9-, TLR11-, ASC-, or RICK-deficient cells but still relied on the adaptor MyD88. These studies demonstrate a transition in the intestinal microflora accompanied by a dynamic change of its ability to stimulate different PRRs which control intestinal homeostasis.

Indexed as

AnimalsBone Marrow CellsImmune SystemImmunity, InnateIntestinal MucosaMacrophagesMiceMice, KnockoutMouth MucosaReceptors, Pattern RecognitionReceptors, Pattern Recognition

Identifiers

PMID19933833
PMCPMC2812188
OpenAlexW2100874193

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.