Evidence map›Paper›PMID 23137965›Full record

ReviewGut microbes

The influence of commensal bacteria-derived signals on basophil-associated allergic inflammation.

David A Hill, David Artis

Open access · bronzeAbstract readReview
In one paragraph

Review in Gut microbes. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. The Microbiome and Food Allergy.Annual review of immunology · 2019
    Review
  4. Microbiome Dependent Regulation of TFrontiers in immunology · 2019
    Review
  5. Article
  6. Role of Short Chain Fatty Acids in Controlling TFrontiers in microbiology · 2018
    Article
  7. Review
  8. New insights into basophil heterogeneity.Seminars in immunopathology · 2016
    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

2 authors at 2 institutions in 2 countries.

David A HillDepartment of Microbiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
David Artis
Philadelphia University · USUniversity of Pennsylvania · US

Funding

UNIVERSITY OF PENNSYLVANIA CAN CTR SUPPORT GRANTP30CA016520 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Susan M Domchek · 1985 to 2026
$222.3M
TRANSGENIC AND CHIMERIC MOUSE COREP30DK050306 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Ken Hashigiwa Cadwell · 1997 to 2026
$32.5M
Regulation of protective immunity following enteric viral infectionU01AI095608 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI ARTIS, DAVID, SONNENBERG, GREGORY F · 2011 to 2025
$11.0M
Innate immunity and inflammation following helminth infectionR01AI074878 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI ARTIS, DAVID · 2008 to 2019
$4.2M
Immuno-regulation of GI nematode infectionR01AI061570 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI ARTIS, DAVID · 2004 to 2013
$4.1M
Regulation and function of innate lymphoid cells in the gutR01AI095466 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI ARTIS, DAVID · 2011 to 2022
$3.7M
Cytokine regulation of anti-helminth immunityR01AI097333 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI ARTIS, DAVID · 2012 to 2016
$2.0M
Training in bacteriologyT32AI060516 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI GOULIAN, MARK D, ZHU, JUN · 2006 to 2015
$2.0M
Functional Biology of Intestinal Epithelial Cells in Food AllergyR21AI087990 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI ARTIS, DAVID, ZIEGLER, STEVEN F · 2010 to 2011
$484k
Epithelial cell regulation of intestinal immune homeostasisR21AI083480 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI ARTIS, DAVID · 2009 to 2010
$436k
NCI NIH HHS 2-P30 CA016520NCI NIH HHS P30 CA016520NIAID NIH HHS AI061570NIAID NIH HHS AI074878NIAID NIH HHS AI083480NIAID NIH HHS AI087990NIAID NIH HHS AI095466NIAID NIH HHS AI095608NIAID NIH HHS AI097333NIAID NIH HHS R01 AI061570NIAID NIH HHS R01 AI074878NIAID NIH HHS R01 AI095466NIAID NIH HHS R01 AI097333NIAID NIH HHS R21 AI083480NIAID NIH HHS R21 AI087990NIAID NIH HHS T32 AI060516NIAID NIH HHS U01 AI095608NIDDK NIH HHS P30 DK050306NIDDK NIH HHS P30-DK050306
6 · The paper itself

Abstract

Commensal bacteria that colonize mammalian mucosal surfaces are reported to influence T helper type 2 (TH 2) cytokine-dependent inflammation and susceptibility to allergic disease. However, the mechanisms that underlie these observations are only beginning to be understood. We recently utilized studies of murine model systems and atopic patient populations to elucidate a mechanism by which commensal bacteria-derived signals limit serum immunoglobulin E levels, influence basophil development and steady-state circulating basophil populations and regulate basophil-associated TH 2 cell responses and allergic inflammation. In this addendum, we summarize the findings of our recent work and other developments in the field, discuss the broader implications of these findings and generate new hypotheses regarding our understanding of host-commensal relationships. These areas of investigation may be applicable to the development of new preventative or therapeutic approaches to reduce the burden of allergic disease.

Indexed as

InflammationAnimalsBacteriaBasophilsDisease Models, AnimalHypersensitivityMiceTh2 Cellsallergyatopybasophilcommensal bacteriahematopoiesis

Identifiers

PMID23137965
PMCPMC3555891
OpenAlexW2005626415

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.