Evidence map›Paper›PMID 30876905›Full record

ReviewExperimental neurology2019

The emerging role of neutrophils as modifiers of recovery after traumatic injury to the developing brain.

Ramona E von Leden, Kaila N Parker, Adrian A Bates, Linda J Noble-Haeusslein, Michael H Donovan

Open access · greenAbstract readReview
In one paragraph

Review in Experimental neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

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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 1 institution in 1 country.

Ramona E von LedenDepartment of Neurology, Dell Medical School, The University of Texas at Austin, 1701 Trinity St., Austin, TX 78712, USA. Electronic address: ramona.von-leden@austin.utexas.edu.
Kaila N ParkerDepartment of Psychology, Behavioral Neuroscience, The University of Texas at Austin, 108 E. Dean Keeton St., Austin, TX 78712, USA. Electronic address: parkerk@utexas.edu.
Adrian A BatesInstitute for Neuroscience, The University of Texas at Austin, 100 E. 24(th) St., Austin, TX 78712, USA. Electronic address: abates@wellesley.edu.
Linda J Noble-HaeussleinDepartment of Neurology, Dell Medical School, The University of Texas at Austin, 1701 Trinity St., Austin, TX 78712, USA; Department of Psychology, Behavioral Neuroscience, The University of Texas at Austin, 108 E. Dean Keeton St., Austin, TX 78712, USA; Institute for Neuroscience, The University of Texas at Austin, 100 E. 24(th) St., Austin, TX 78712, USA. Electronic address: linda.noble@austin.utexas.edu.
Michael H DonovanDepartment of Neurology, Dell Medical School, The University of Texas at Austin, 1701 Trinity St., Austin, TX 78712, USA. Electronic address: michael.donovan@austin.utexas.edu.
The University of Texas at Austin · US

Funding

Trauma to Developing Brain-Injury and Repair MechanismsR01NS050159 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NOBLE, LINDA J. · 2005 to 2013
$2.8M
Determinants of vulnerability and recovery after trauma to the developing brainR01NS077767 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NOBLE, LINDA J. · 2012 to 2016
$1.7M
NINDS NIH HHS R01 NS050159NINDS NIH HHS R01 NS077767
6 · The paper itself

Abstract

The innate immune response plays a critical role in traumatic brain injury (TBI), contributing to ongoing pathogenesis and worsening long-term outcomes. Here we focus on neutrophils, one of the "first responders" to TBI. These leukocytes are recruited to the injured brain where they release a host of toxic molecules including free radicals, proteases, and pro-inflammatory cytokines, all of which promote secondary tissue damage. There is mounting evidence that the developing brain is more vulnerable to injury that the adult brain. This vulnerability to greater damage from TBI is, in part, attributed to relatively low antioxidant reserves coupled with an early robust immune response. The latter is reflected in enhanced sensitivity to cytokines and a prolonged recruitment of neutrophils into both cortical and subcortical regions. This review considers the contribution of neutrophils to early secondary pathogenesis in the injured developing brain and raises the distinct possibility that these leukocytes, which exhibit phenotypic plasticity, may also be poised to support wound healing. We provide a basic review of the development, life cycle, and granular contents of neutrophils and evaluate their potential as therapeutic targets for early neuroprotection and functional recovery after injury at early age. While neutrophils have been broadly studied in neurotrauma, we are only beginning to appreciate their diverse roles in the developing brain and the extent to which their acute manipulation may result in enduring neurological recovery when TBI is superimposed upon brain development.

Indexed as

Neutrophil InfiltrationAdolescentAnimalsBrain Injuries, TraumaticChildChild, PreschoolHumansInfantInfant, NewbornNeutrophilsRecovery of FunctionGranulesNeutropeniaNeutrophil elastaseOxidative stressPolarizationRecruitment

Identifiers

PMID30876905
PMCPMC6544477
OpenAlexW2921006384

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.