Evidence map›Paper›PMID 29648974›Full record

ArticleJournal of neurotrauma2018

Traumatic Brain Injury-Induced Acute Lung Injury: Evidence for Activation and Inhibition of a Neural-Respiratory-Inflammasome Axis.

Nadine A Kerr, Juan Pablo de Rivero Vaccari, Sam Abbassi, Harmanpreet Kaur, Ronald Zambrano, Shu Wu, W Dalton Dietrich, Robert W Keane

Abstract read
In one paragraph

Article in Journal of neurotrauma, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

78 citing papers in PubMed, 107 citations in OpenAlex.

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18 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

8 authors at 2 institutions in 1 country.

Nadine A Kerr1 Department of Neurological Surgery, University of Miami Miller School of Medicine , Miami, Florida.
Juan Pablo de Rivero Vaccari1 Department of Neurological Surgery, University of Miami Miller School of Medicine , Miami, Florida.
Sam Abbassi2 Department of Physiology and Biophysics, University of Miami Miller School of Medicine , Miami, Florida.
Harmanpreet Kaur1 Department of Neurological Surgery, University of Miami Miller School of Medicine , Miami, Florida.
Ronald Zambrano3 Department of Pediatrics, University of Miami Miller School of Medicine , Miami, Florida.
Shu Wu3 Department of Pediatrics, University of Miami Miller School of Medicine , Miami, Florida.
W Dalton Dietrich1 Department of Neurological Surgery, University of Miami Miller School of Medicine , Miami, Florida.
Robert W Keane1 Department of Neurological Surgery, University of Miami Miller School of Medicine , Miami, Florida.
University of Miami · USNeurological Surgery · US

Funding

The Importance of Temperature on Inflammation after TBIR01NS042133 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI DIETRICH, W DALTON · 2002 to 2020
$5.0M
Therapeutic Neutralization of the Inflammasome After Spinal Cord InjuryR42NS086274 · NINDS · INFLAMACORE, LLC · PI KEANE, ROBERT W · 2014 to 2016
$1.5M
NINDS NIH HHS R01 NS042133NINDS NIH HHS R42 NS086274
6 · The paper itself

Abstract

Approximately 20-25% of traumatic brain injury (TBI) subjects develop acute lung injury (ALI), but the pathomechanisms of TBI-induced ALI remain poorly defined. Our previous work has shown that the inflammasome plays a critical role in TBI-induced secondary pathophysiology and that inflammasome proteins are released in extracellular vesicles (EV) after TBI. Here we investigated whether EV-mediated inflammasome signaling contributed to the etiology of TBI-induced ALI. C57/BL6 male mice were subjected to controlled cortical impact (CCI), and the brains and lungs were examined for inflammasome activation and ALI at 4 and 24 h after TBI. We show that TBI releases EV containing inflammasome proteins into serum that target the lung to cause ALI, supporting activation of a neural-respiratory-inflammasome axis. Administration of a low-molecular-weight heparin (enoxaparin, a blocker of EV uptake) or treatment with a monoclonal antibody against apoptosis speck-like staining protein containing a caspase recruitment domain (anti-ASC) after adoptive transfer of EV isolated from TBI-injured mice significantly inhibited inflammasome activation in the lungs of recipient mice resulting in improved ALI scores.This axis constitutes an important arm of the innate inflammatory response in lung pathology after TBI and targeting this axis represents a novel therapeutic treatment for TBI-induced ALI.

Indexed as

InflammasomesAcute Lung InjuryAnimalsAnticoagulantsApoptosis Regulatory ProteinsBrain Injuries, TraumaticDNA-Binding ProteinsEnoxaparinExtracellular SpaceHMGB1 ProteinImmunity, InnateMaleMiceMice, Inbred C57BLNervous SystemRespiratory SystemAim2 protein, mouseAnticoagulantsApoptosis Regulatory ProteinsDNA-Binding ProteinsEnoxaparinHMGB1 ProteinHMGB1 protein, mouseInflammasomesacute lung injuryextracellular vesiclesinflammasomeinnate immune responsetraumatic brain injury

Identifiers

PMID29648974
PMCPMC6098413
OpenAlexW2794855561

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.