Evidence map›Paper›PMID 22580716›Full record

ArticlePediatric research2012

Innate immune activation in neonatal tracheal aspirates suggests endotoxin-driven inflammation.

Katheryn E Nathe, Christy J Mancuso, Richard Parad, Linda J Van Marter, Camilia R Martin, Liat Stoler-Barak, Victoria J Philbin, Michele F Phillips, Christine D Palmer, Ofer Levy

Open access · hybridAbstract read
In one paragraph

Article in Pediatric research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 24% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Tracheal aspirate transcriptomic and miRNA signatures of extreme premature birth with bronchopulmonary dysplasia.Journal of perinatology : official journal of the California Perinatal Association · 2021
    Article
  4. Article
  5. Article
  6. Review
  7. Article
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

10 authors at 3 institutions in 1 country.

Katheryn E NatheDepartment of Medicine, Children's Hospital Boston, Massachusetts, USA.
Christy J Mancuso
Richard Parad
Linda J Van Marter
Camilia R Martin
Liat Stoler-Barak
Victoria J Philbin
Michele F Phillips
Christine D Palmer
Ofer Levy
Boston Children's Hospital · USHarvard University · USBrigham and Women's Hospital · US

Funding

Adenosine Shapes Neonatal Toll-like Receptor FunctionR01AI067353 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI LEVY, OFER · 2006 to 2010
$2.1M
SCHOLARS IN CLINICAL SCIENCE PROGRAMK30RR022292 · NCRR · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WILLIAMS, GORDON H · 2005 to 2007
$900k
NCRR NIH HHS K30 RR022292-07NHLBI NIH HHS HL72931NIAID NIH HHS R01 AI067353-01A1
6 · The paper itself

Abstract

backgroundTracheal aspirates (TAs) from critically ill neonates accumulate bacterial endotoxin and demonstrate mobilization of endotoxin-binding proteins, but the potential bioactivity of endotoxin in TAs is unknown. We characterized innate immune activation in TAs of mechanically ventilated neonates.

methodsInnate immune activation in TAs of mechanically ventilated neonates was characterized using a targeted 84-gene quantitative real-time (qRT) PCR array. Protein expression of cytokines was confirmed by multiplex assay. Expression and localization of the endotoxin-inducible antimicrobial protein Calgranulin C (S100A12) was assessed by flow cytometry. Endotoxin levels were measured in TA supernatants using the Limulus amoebocyte lysate assay.

resultsAnalyses by qRT-PCR demonstrated expression of pattern recognition receptors, Toll-like receptor-nuclear factor κB and inflammasome pathways, cytokines/chemokines and their receptors, and anti-infective proteins in TA cells. Endotoxin positivity increased with postnatal age. As compared with endotoxin-negative TAs, endotoxin-positive TAs demonstrated significantly greater tumor necrosis factor (TNF), interleukin (IL)-6, IL-10, and serpin peptidase inhibitor, clade E, member 1 (SERPINE1) mRNA, and IL-10, TNF, and IL-1β protein. Expression of S100A12 protein was localized to TA neutrophils.

conclusionCorrelation of endotoxin with TA inflammatory responses suggests endotoxin bioactivity and the possibility that endotoxin antagonists could mitigate pulmonary inflammation and its sequelae in this vulnerable population.

Indexed as

Age FactorsAnalysis of VarianceCytokinesEndotoxinsFlow CytometryHumansImmunity, InnateInfant, NewbornLimulus TestMicroscopy, FluorescenceReal-Time Polymerase Chain ReactionRespiration, ArtificialS100A12 ProteinS100 ProteinsTracheaCytokinesEndotoxinsS100A12 ProteinS100A12 protein, humanS100 Proteins

Identifiers

PMID22580716
PMCPMC3406551
OpenAlexW2060382496

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.