Evidence map›Paper›PMID 30557659›Full record

ArticleNeurobiology of disease2019

Following spinal cord injury, PDE4B drives an acute, local inflammatory response and a chronic, systemic response exacerbated by gut dysbiosis and endotoxemia.

Scott A Myers, Leila Gobejishvili, Sujata Saraswat Ohri, C Garrett Wilson, Kariena R Andres, Amberly S Riegler, Hridgandh Donde, Swati Joshi-Barve, Shirish Barve, Scott R Whittemore

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurobiology of disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 3 pooled it
3.6field-weighted citation impact, top 6% 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

54 citing papers in PubMed, 3 syntheses or guidelines pooled it, 84 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

10 authors at 2 institutions in 1 country.

Scott A MyersKentucky Spinal Cord Injury Research Center, University of Louisville, School of Medicine, 511 S. Floyd St., MDR 616, Louisville, KY 40202, USA; Department of Neurological Surgery, University of Louisville, School of Medicine, 511 S. Floyd St., MDR 616, Louisville, KY 40202, USA.
Leila GobejishviliDepartments of Internal Medicine and Pharmacology and Toxicology, and Alcohol Research Center, University of Louisville, School of Medicine, 505 South Hancock Street, CTR Building, Room 515, Louisville, KY 40202, USA.
Sujata Saraswat OhriKentucky Spinal Cord Injury Research Center, University of Louisville, School of Medicine, 511 S. Floyd St., MDR 616, Louisville, KY 40202, USA; Department of Neurological Surgery, University of Louisville, School of Medicine, 511 S. Floyd St., MDR 616, Louisville, KY 40202, USA.
C Garrett WilsonUAB School of Medicine, University of Alabama at Birmingham, Bevill Biomedical Research Building, Birmingham, AL 35294, USA.
Kariena R AndresKentucky Spinal Cord Injury Research Center, University of Louisville, School of Medicine, 511 S. Floyd St., MDR 616, Louisville, KY 40202, USA; Department of Neurological Surgery, University of Louisville, School of Medicine, 511 S. Floyd St., MDR 616, Louisville, KY 40202, USA.
Amberly S RieglerKentucky Spinal Cord Injury Research Center, University of Louisville, School of Medicine, 511 S. Floyd St., MDR 616, Louisville, KY 40202, USA; Department of Neurological Surgery, University of Louisville, School of Medicine, 511 S. Floyd St., MDR 616, Louisville, KY 40202, USA.
Hridgandh DondeDepartments of Internal Medicine and Pharmacology and Toxicology, and Alcohol Research Center, University of Louisville, School of Medicine, 505 South Hancock Street, CTR Building, Room 515, Louisville, KY 40202, USA.
Swati Joshi-BarveDepartments of Internal Medicine and Pharmacology and Toxicology, and Alcohol Research Center, University of Louisville, School of Medicine, 505 South Hancock Street, CTR Building, Room 515, Louisville, KY 40202, USA.
Shirish BarveDepartments of Internal Medicine and Pharmacology and Toxicology, and Alcohol Research Center, University of Louisville, School of Medicine, 505 South Hancock Street, CTR Building, Room 515, Louisville, KY 40202, USA. Electronic address: Shirish.barve@louisville.edu.
Scott R WhittemoreKentucky Spinal Cord Injury Research Center, University of Louisville, School of Medicine, 511 S. Floyd St., MDR 616, Louisville, KY 40202, USA; Department of Neurological Surgery, University of Louisville, School of Medicine, 511 S. Floyd St., MDR 616, Louisville, KY 40202, USA; Department of Anatomical Science & Neurobiology, University of Louisville, School of Medicine, 511 S. Floyd St., MDR 616, Louisville, KY 40202, USA. Electronic address: swhittemore@louisville.edu.
University of Louisville · USUniversity of Alabama at Birmingham · US

Funding

Vascular responses as therapeutic targets after SCIR01NS045734 · NINDS · UNIVERSITY OF LOUISVILLE · PI HAGG, THEO, WHITTEMORE, SCOTT R · 2004 to 2015
$5.0M
Role of Gut Microbiome and DHA Deficiency in Alcohol Induced NeuroinflammationU01AA022618 · NIAAA · UNIVERSITY OF LOUISVILLE · PI BARVE, SHIRISH S · 2016 to 2020
$1.7M
SAM Deficiency Mediated Epigenetic Mechanisms in Alcohol induced ImmunosuppressionR01AA024405 · NIAAA · UNIVERSITY OF LOUISVILLE · PI BARVE, SHIRISH S · 2015 to 2019
$1.6M
The role of hepatocyte cAMP/PDE4 in alcohol-induced liver steatosis and injuryR21AA022189 · NIAAA · UNIVERSITY OF LOUISVILLE · PI GOBEJISHVILI, LEILA · 2014 to 2015
$388k
NIAAA NIH HHS R01 AA024405NIAAA NIH HHS R21 AA022189NIAAA NIH HHS U01 AA022618NINDS NIH HHS R01 NS045734
6 · The paper itself

Abstract

Emerging evidence links changes in the gut microbiome and intestinal barrier function to alterations in CNS function. We examined the role of endotoxin-responsive, cAMP-specific, Pde4 subfamily b (Pde4b) enzyme in gut dysbiosis induced neuro-inflammation and white matter loss following spinal cord injury (SCI). Using a thoracic contusion model in C57Bl/6 wild type female mice, SCI led to significant shifts in the gut bacterial community including an increase in the phylum Proteobacteria, which consists of endotoxin-harboring, gram-negative bacteria. This was accompanied by increased systemic inflammatory marker, soluble CD14, along with markers of the endoplasmic reticulum stress response (ERSR) and inflammation in the SCI epicenter. Deletion of Pde4b reduced epicenter expression of markers for the ERSR and inflammation, at both acute and chronic time points post-SCI. Correspondingly, expression of oligodendrocyte mRNAs increased. Within the injury penumbra, inflammatory protein markers of activated astrocytes (GFAP), macrophage/microglia (CD11b, Iba1), and the proinflammatory mediator Cox2, were decreased in Pde4b

Indexed as

AnimalsCyclic Nucleotide Phosphodiesterases, Type 4DysbiosisEndoplasmic Reticulum StressEndotoxemiaFemaleInflammationMiceMice, Inbred C57BLMice, KnockoutRecovery of FunctionSpinal Cord InjuriesCyclic Nucleotide Phosphodiesterases, Type 4PDE4B protein, mouseEndotoxemiaER stress responseGut dysbiosisInflammationPhosphodiesterase 4B2Spinal cord injury

Identifiers

PMID30557659
PMCPMC6445388
OpenAlexW2905247497

What OpenQuestion holds

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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.