Evidence map›Paper›PMID 30105286›Full record

ReviewCellular and molecular gastroenterology and hepatology2018

Toll-Like Receptor-Mediated Intestinal Inflammatory Imbalance in the Pathogenesis of Necrotizing Enterocolitis.

David J Hackam, Chhinder P Sodhi

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cellular and molecular gastroenterology and hepatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed, 3 pooled it
8.8field-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

118 citing papers in PubMed, 3 syntheses or guidelines pooled it, 179 citations in OpenAlex.

  1. Pooled it
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  10. Effects of specialized proresolving mediators on gut epithelial barrier in early life.The Journal of pharmacology and experimental therapeutics · 2026
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  14. Is necrotizing enterocolitis associated with the 896A/G polymorphism in the toll-like receptor 4 (TLR4) gene?Arquivos brasileiros de cirurgia digestiva : ABCD = Brazilian archives of digestive surgery · 2026
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58 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

2 authors at 2 institutions in 1 country.

David J HackamDivision of General Pediatric Surgery, Johns Hopkins University, Johns Hopkins Hospital, Baltimore, Maryland.
Chhinder P SodhiDivision of General Pediatric Surgery, Johns Hopkins University, Johns Hopkins Hospital, Baltimore, Maryland.
Johns Hopkins Children's Center · USJohns Hopkins University · 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
NIDDK NIH HHS R01 DK083752NIGMS NIH HHS R01 GM078238
6 · The paper itself

Abstract

Necrotizing enterocolitis (NEC) remains the leading cause of death from gastrointestinal disease in premature infants and attacks the most fragile patients at a time when they appear to be the most stable. Despite significant advances in our overall care of the premature infant, NEC mortality remains stubbornly high. There is no specific treatment for NEC beyond broad-spectrum antibiotics and intestinal resection, and current efforts have focused on preventive strategies. Over the past decade, we have proposed a unifying hypothesis to explain the pathogenesis of NEC in premature infants that suggests that NEC develops in response to an imbalance between exaggerated proinflammatory signaling in the mucosa of the premature gut leading to mucosal injury, which is not countered effectively by endogenous repair processes, and in the setting of impaired mesenteric perfusion leads to intestinal ischemia and disease development. One of the most important pathways that mediates the balance between injury and repair in the premature intestine, and that plays a key role in NEC pathogenesis, is Toll-like receptor 4 (TLR4), which recognizes lipopolysaccharide on gram-negative bacteria. This review focuses on the role that the TLR4-mediated imbalance between proinflammatory and anti-inflammatory signaling in the premature intestinal epithelium leads to the development of NEC, and will explore how an understanding of the role of TLR4 in NEC pathogenesis has led to the identification of novel preventive or treatment approaches for this devastating disease.

Indexed as

Enterocolitis, NecrotizingHumansInfantInfant, NewbornInfant, PrematureInfant, Premature, DiseasesInflammationIntestinal MucosaMilk, HumanMortality, PrematureRisk FactorsToll-Like Receptor 4TLR4 protein, humanToll-Like Receptor 4EnterocytelneonateLPS, lipopolysaccharideMicrobiomeNEC, necrotizing enterocolitisNutritionProbioticSepsisTLR4, Toll-like receptor 4TLR, Toll-like receptor

Identifiers

PMID30105286
PMCPMC6085538
OpenAlexW2795552079

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.