Evidence map›Paper›PMID 26577908›Full record

ReviewJournal of pediatric surgery2016

Roles of nitric oxide and intestinal microbiota in the pathogenesis of necrotizing enterocolitis.

Anatoly Grishin, Jordan Bowling, Brandon Bell, Jin Wang, Henri R Ford

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of pediatric surgery, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 2 pooled it
5.9field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 2 syntheses or guidelines pooled it, 74 citations in OpenAlex.

  1. Pooled it
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  12. A Combination of Polymethoxyflavones fromAntioxidants (Basel, Switzerland) · 2023
    Article
  13. Update on the Pathogenesis of the Hirschsprung-Associated Enterocolitis.International journal of molecular sciences · 2023
    Review
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  15. 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

5 authors at 2 institutions in 1 country.

Anatoly GrishinDivision of Pediatric Surgery, Children's Hospital Los Angeles, 4650 Sunset Boulevard, Los Angeles, CA 90027; Department of Surgery, Keck School of Medicine of the University of Southern California, 4650 Sunset Boulevard, Los Angeles, CA 90027. Electronic address: agrishin@chla.usc.edu.
Jordan BowlingDepartment of Surgery, Keck School of Medicine of the University of Southern California, 4650 Sunset Boulevard, Los Angeles, CA 90027. Electronic address: jbowling@chla.usc.edu.
Brandon BellDivision of Pediatric Surgery, Children's Hospital Los Angeles, 4650 Sunset Boulevard, Los Angeles, CA 90027. Electronic address: bbell@chla.usc.edu.
Jin WangDivision of Pediatric Surgery, Children's Hospital Los Angeles, 4650 Sunset Boulevard, Los Angeles, CA 90027. Electronic address: jinwang@chla.usc.edu.
Henri R FordDivision of Pediatric Surgery, Children's Hospital Los Angeles, 4650 Sunset Boulevard, Los Angeles, CA 90027; Department of Surgery, Keck School of Medicine of the University of Southern California, 4650 Sunset Boulevard, Los Angeles, CA 90027. Electronic address: hford@chla.usc.edu.
University of Southern California · USChildren's Hospital of Los Angeles · US

Funding

PATHOGENESIS AND TREATMENT OF EXPERIMENTAL PERITONITISR01AI014032 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FORD, HENRI R · 1985 to 2014
$3.4M
NIAID NIH HHS R01 AI 014032NIAID NIH HHS R01 AI014032
6 · The paper itself

Abstract

Necrotizing enterocolitis remains one of the most vexing problems in the neonatal intensive care unit. Risk factors for NEC include prematurity, formula feeding, and inappropriate microbial colonization of the GI tract. The pathogenesis of NEC is believed to involve weakening of the intestinal barrier by perinatal insults, translocation of luminal bacteria across the weakened barrier, an exuberant inflammatory response, and exacerbation of the barrier damage by inflammatory factors, leading to a vicious cycle of inflammation-inflicted epithelial damage. Nitric oxide (NO), produced by inducible NO synthase (iNOS) and reactive NO oxidation intermediates play a prominent role in the intestinal barrier damage by inducing enterocyte apoptosis and inhibiting the epithelial restitution processes, namely enterocyte proliferation and migration. The factors that govern iNOS upregulation in the intestine are not well understood, which hampers efforts in developing NO/iNOS-targeted therapies. Similarly, efforts to identify bacteria or bacterial colonization patterns associated with NEC have met with limited success, because the same bacterial species can be found in NEC and in non-NEC subjects. However, microbiome studies have identified the three important characteristics of early bacterial populations of the GI tract: high diversity, low complexity, and fluidity. Whether NEC is caused by specific bacteria remains a matter of debate, but data from hospital outbreaks of NEC strongly argue in favor of the infectious nature of this disease. Studies in Cronobacter muytjensii have established that the ability to induce NEC is the property of specific strains rather than the species as a whole. Progress in our understanding of the roles of bacteria in NEC will require microbiological experiments and genome-wide analysis of virulence factors.

Indexed as

Gastrointestinal MicrobiomeBiomarkersEnterocolitis, NecrotizingHumansInfant, NewbornIntestinal MucosaNitric OxidePermeabilityBiomarkersNitric OxideBacteriaGut barrierNecrotizing enterocolitisNitric oxide

Identifiers

PMID26577908
PMCPMC4894644
OpenAlexW2191597877

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.