Evidence map›Paper›PMID 23238281›Full record

ArticleJournal of theoretical biology2013

Modeling the interactions of bacteria and Toll-like receptor-mediated inflammation in necrotizing enterocolitis.

Julia Arciero, G Bard Ermentrout, Richard Siggers, Amin Afrazi, David Hackam, Yoram Vodovotz, Jonathan Rubin

Abstract read
In one paragraph

Article in Journal of theoretical biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  5. Nutrients · 2021
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  11. Mesenchymal stem cells cannot affect mRNA expression of toll-like receptors in different tissues during sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
    Article
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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

7 authors at 3 institutions in 1 country.

Julia ArcieroDepartment of Mathematics, IUPUI, Indianapolis, IN 46202, USA. jarciero@math.iupui.edu
G Bard Ermentrout
Richard Siggers
Amin Afrazi
David Hackam
Yoram Vodovotz
Jonathan Rubin
University of Pittsburgh · USIndiana University – Purdue University Indianapolis · USMcGowan Institute for Regenerative Medicine · US

Funding

TLR4 Signaling in the Pathogenesis of Surgical Necrotizing EnterocolitisR01GM078238 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HACKAM, DAVID J · 2006 to 2019
$3.9M
Modulation of TLR4 and TLR9 Signaling in NECR01DK083752 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HACKAM, DAVID J · 2008 to 2016
$3.4M
Regulation of TLR4 Signaling in Enterocytes in Necrotizing EnterocolitisF30DK085930 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AFRAZI, AMIN · 2009 to 2013
$234k
NIDDK NIH HHS F30 DK085930NIDDK NIH HHS R01 DK083752NIGMS NIH HHS R01 GM078238
6 · The paper itself

Abstract

Necrotizing enterocolitis (NEC) is a severe disease of the gastrointestinal tract in premature infants, characterized by a disrupted intestinal epithelium and an exaggerated pro-inflammatory response. Since the activation of Toll-like receptor-4 (TLR4) blocks cell migration and proliferation and contributes to an uncontrolled inflammatory response within the intestine, this receptor has been identified as a key contributor to the development of NEC. Toll-like receptor-9 (TLR9) has been shown to sense bacterial genome components (CpG DNA) and to play an anti-inflammatory role in NEC. We present in vitro results demonstrating direct inhibition of TLR4 activation by CpG DNA, and we develop a mathematical model of bacteria-immune interactions within the intestine to investigate how such inhibition of TLR4 signaling might alter inflammation, associated bacterial invasion of tissue, and resulting outcomes. The model predicts that TLR9 can inhibit both the beneficial and detrimental effects of TLR4, and thus a proper balance of action by these two receptors is needed to promote intestinal health. The model results are also used to explore three interventions that could potentially prevent the development of NEC: reducing bacteria in the mucus layer, administering probiotic treatment, and blocking TLR4 activation. While the model shows that these interventions would be successful in most cases, the model is also used to identify situations in which the proposed treatments might be harmful.

Indexed as

AnimalsBacteriaCell LineComputer SimulationCpG IslandsDNAEnterocolitis, NecrotizingEpithelial CellsHumansInflammationIntestinesModels, BiologicalToll-Like ReceptorsDNAToll-Like Receptors

Identifiers

PMID23238281
PMCPMC4893796
OpenAlexW2022330584

What OpenQuestion holds

Textmetadata
LicenceTDM
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.