Evidence map›Paper›PMID 31640184›Full record

ArticleViruses2019

Gut DNA Virome Diversity and Its Association with Host Bacteria Regulate Inflammatory Phenotype and Neuronal Immunotoxicity in Experimental Gulf War Illness.

Ratanesh K Seth, Rabia Maqsood, Ayan Mondal, Dipro Bose, Diana Kimono, LaRinda A Holland, Patricia Janulewicz Lloyd, Nancy Klimas, Ronnie D Horner, Kimberly Sullivan and 2 more

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.5field-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

35 citing papers in PubMed, 53 citations in OpenAlex.

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  17. Gut virome dysbiosis following focal cerebral ischemia in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022
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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

12 authors at 5 institutions in 1 country.

Ratanesh K SethEnvironmental Health and Disease Laboratory, Department of Environmental Health Sciences, University of South Carolina, Columbia, SC 29208, USA. sethr@mailbox.sc.edu.ORCID 0000-0002-7078-0052
Rabia MaqsoodCenter for Fundamental and Applied Microbiomics, The Biodesign Institute, Arizona State University, Tempe, AZ 85281, USA. Rabia.Maqsood@asu.edu.
Ayan MondalEnvironmental Health and Disease Laboratory, Department of Environmental Health Sciences, University of South Carolina, Columbia, SC 29208, USA. mondola@mailbox.sc.edu.
Dipro BoseEnvironmental Health and Disease Laboratory, Department of Environmental Health Sciences, University of South Carolina, Columbia, SC 29208, USA. bosed@email.sc.edu.
Diana KimonoEnvironmental Health and Disease Laboratory, Department of Environmental Health Sciences, University of South Carolina, Columbia, SC 29208, USA. Dkimono@email.sc.edu.
LaRinda A HollandCenter for Fundamental and Applied Microbiomics, The Biodesign Institute, Arizona State University, Tempe, AZ 85281, USA. LaRinda.Holland@asu.edu.
Patricia Janulewicz LloydSchool of Public Health, Boston University, Boston MA 02118, USA. paj@bu.edu.
Nancy KlimasNOVA Southeastern University, Fort Lauderdale, FL 33314, USA. nklimas@nova.edu.
Ronnie D HornerDepartment of Health Services Policy and Management, University of South Carolina, Columbia, SC 29208, USA. hornerrd@mailbox.sc.edu.
Kimberly SullivanSchool of Public Health, Boston University, Boston MA 02118, USA. tty@bu.edu.ORCID 0000-0001-7940-6123
Efrem S LimCenter for Fundamental and Applied Microbiomics, The Biodesign Institute, Arizona State University, Tempe, AZ 85281, USA. Efrem.Lim@asu.edu.ORCID 0000-0002-3397-9310
Saurabh ChatterjeeEnvironmental Health and Disease Laboratory, Department of Environmental Health Sciences, University of South Carolina, Columbia, SC 29208, USA. schatt@mailbox.sc.edu.
South Carolina Department of Health and Environmental Control · USArizona State University · USBoston University · USNova Southeastern University · USUniversity of South Carolina · US

Funding

Targeting early ceramide elevation in pre-symptomatic eczemaP20GM103641 · NIGMS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI ENOS, REILLY, NAGARKATTI, PRAKASH S · 2012 to 2023
$20.7M
Use of Resveratrol to treat experimental multiple sclerosisP01AT003961 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI NAGARKATTI, PRAKASH S · 2007 to 2018
$14.2M
The Virome and Microbiome in Health and BK Disease of Kidney Transplant PatientsR00DK107923 · NIDDK · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · PI LIM, EFREM · 2017 to 2019
$747k
Free Radical Mechanism in Obesity Potentiation of Environmental HepatotoxicityR00ES019875 · NIEHS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI CHATTERJEE, SAURABH · 2012 to 2014
$747k
CMA: Immune/Inflammatory Priming in Exacerbating Responses to GWVI Stressors: Implications for GWVI TreatmentsI01CX001923 · VA · VETERANS HEALTH ADMINISTRATION · PI Saurabh Chatterjee · 2019 to 2026
–
CSRD VA I01 CX001923NCCIH NIH HHS P01 AT003961NIDDK NIH HHS R00 DK107923NIEHS NIH HHS R00 ES019875NIGMS NIH HHS P20 GM103641VA CX001923-01
6 · The paper itself

Abstract

Gulf War illness (GWI) is characterized by the persistence of inflammatory bowel disease, chronic fatigue, neuroinflammation, headache, cognitive impairment, and other medically unexplained conditions. Results using a murine model show that enteric viral populations especially bacteriophages were altered in GWI. The increased viral richness and alpha diversity correlated positively with gut bacterial dysbiosis and proinflammatory cytokines. Altered virome signature in GWI mice also had a concomitant weakening of intestinal epithelial tight junctions with a significant increase in Claudin-2 protein expression and decrease in ZO1 and Occludin mRNA expression. The altered virome signature in GWI, decreased tight junction protein level was followed by the presence an activation of innate immune responses such as increased Toll-like receptor (TLR) signaling pathways. The altered virome diversity had a positive correlation with serum IL-6, IL-1β, and IFN-γ, intestinal inflammation (IFN-γ), and decreased Brain-Derived Neurotrophic Factor (BDNF), a neurogenesis marker. The co-exposure of Gulf War chemical and antibiotic (for gut sterility) or Gulf War chemical and Ribavirin, an antiviral compound to suppress virus alteration in the gut showed significant improvement in epithelial tight junction protein, decreased intestinal-, systemic-, and neuroinflammation. These results showed that the observed enteric viral dysbiosis could activate enteric viral particle-induced innate immune response in GWI and could be a novel therapeutic target in GWI.

Indexed as

Gastrointestinal MicrobiomePersian Gulf SyndromeAnimalsAntiviral AgentsBacteriaCytokinesDisease Models, AnimalDNADysbiosisImmunity, InnateInflammationMaleMiceMice, Inbred C57BLNeuronsPermethrinAntiviral AgentsCytokinesDNAPermethrinPyridostigmine BromideRibavirinGulf war illnessIL6intestinal inflammationmicrobiomeneuroinflammationnext-generation sequencingRibavirinVirome

Identifiers

PMID31640184
PMCPMC6832151
OpenAlexW2981255188

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.