Evidence map›Paper›PMID 28705839›Full record

ArticleBlood2017

Circulating dsDNA, endothelial injury, and complement activation in thrombotic microangiopathy and GVHD.

Nicholas J Gloude, Pooja Khandelwal, Nathan Luebbering, Dana T Lounder, Sonata Jodele, Matthew N Alder, Adam Lane, Alyss Wilkey, Kelly E Lake, Bridget Litts and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 5 pooled it
4.6field-weighted citation impact, top 4% 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

74 citing papers in PubMed, 5 syntheses or guidelines pooled it, 112 citations in OpenAlex.

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  20. Kinetics of DNases after hematopoietic stem cell transplant.Blood vessels, thrombosis & hemostasis · 2025
    Article

14 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

11 authors at 2 institutions in 1 country.

Nicholas J GloudeDivision of Bone Marrow Transplantation and Immune Deficiency and.
Pooja KhandelwalDivision of Bone Marrow Transplantation and Immune Deficiency and.
Nathan LuebberingDivision of Bone Marrow Transplantation and Immune Deficiency and.
Dana T LounderDivision of Bone Marrow Transplantation and Immune Deficiency and.
Sonata JodeleDivision of Bone Marrow Transplantation and Immune Deficiency and.
Matthew N AlderDivision of Critical Care Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH.
Adam LaneDivision of Bone Marrow Transplantation and Immune Deficiency and.
Alyss WilkeyDivision of Bone Marrow Transplantation and Immune Deficiency and.
Kelly E LakeDivision of Bone Marrow Transplantation and Immune Deficiency and.
Bridget LittsDivision of Bone Marrow Transplantation and Immune Deficiency and.
Stella M DaviesDivision of Bone Marrow Transplantation and Immune Deficiency and.
Immune Deficiency Foundation · USCincinnati Children's Hospital Medical Center · US

Funding

Pediatric Center--Gene Expression /Developmental ScienceK12HD028827 · NICHD · CINCINNATI CHILDRENS HOSP MED CTR · PI Tina Lee Cheng · 2002 to 2026
$9.6M
NICHD NIH HHS K12 HD028827
6 · The paper itself

Abstract

Transplant-associated thrombotic microangiopathy (TA-TMA) is a common and poorly recognized complication of hematopoietic stem cell transplantation (HSCT) associated with excessive complement activation, likely triggered by endothelial injury. An important missing piece is the link between endothelial injury and complement activation. We hypothesized that neutrophil extracellular traps (NETs) mechanistically link endothelial damage with complement activation and subsequent TA-TMA. Neutrophil activation releases granule proteins together with double-stranded DNA (dsDNA) to form extracellular fibers known as NETs. NETs have been shown to activate complement and can be assessed in humans by quantification of dsDNA in serum. We measured levels of dsDNA, as a surrogate for NETs in 103 consecutive pediatric allogeneic transplant recipients at day 0, +14, +30, +60, and +100. A spike in dsDNA production around day +14 during engraftment was associated with subsequent TA-TMA development. Peak dsDNA production around day +14 was associated with interleukin-8-driven neutrophil recovery. Increased dsDNA levels at days +30, +60, and +100 were also associated with increased mortality and gastrointestinal graft-versus-host disease (GVHD). NETs may serve as a mechanistic link between endothelial injury and complement activation. NET formation may be one mechanism contributing to the clinical overlap between GVHD and TA-TMA.

Indexed as

AdolescentAdultChildChild, PreschoolComplement ActivationDemographyDNAEndothelial CellsExtracellular TrapsGraft vs Host DiseaseHematopoietic Stem Cell TransplantationHumansInfantInterleukin-8Longitudinal StudiesNeutrophilsDNAInterleukin-8Receptors, Interleukin-8AReceptors, Interleukin-8B

Identifiers

PMID28705839
PMCPMC5714230
OpenAlexW2736218182

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.