Evidence map›Paper›PMID 30728013›Full record

ArticleRespiratory research2019

Ethyl pyruvate reduces organic dust-induced airway inflammation by targeting HMGB1-RAGE signaling.

Sanjana Mahadev Bhat, Nyzil Massey, Locke A Karriker, Baljit Singh, Chandrashekhar Charavaryamath

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

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  14. In focus in HCB.Histochemistry and cell biology · 2021
    Article
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  18. Review
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  20. HMGB1-RAGE Signaling Plays a Role in Organic Dust-Induced Microglial Activation and Neuroinflammation.Toxicological sciences : an official journal of the Society of Toxicology · 2019
    Article
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 2 institutions in 2 countries.

Sanjana Mahadev BhatDepartment of Biomedical Sciences, 2008 Vet Med Building, Iowa State University, Ames, IA, USA.
Nyzil MasseyDepartment of Biomedical Sciences, 2008 Vet Med Building, Iowa State University, Ames, IA, USA.
Locke A KarrikerDepartment of Veterinary Diagnostic and Production Animal Medicine, 2203 Lloyd Veterinary Medical Center, Iowa State university, Ames, IA, USA.
Baljit SinghFaculty of Veterinary Medicine, 2500 University Dr. NW, University of Calgary, Calgary, T2N 1N4, Canada.
Chandrashekhar CharavaryamathDepartment of Biomedical Sciences, 2008 Vet Med Building, Iowa State University, Ames, IA, USA. chandru@iastate.edu.ORCID http://orcid.org/0000-0002-5217-1608
Iowa State University · USUniversity of Calgary · CA

Funding

Great Plains Center for Agricultural Health (GPCAH)U54OH007548 · OH · UNIVERSITY OF IOWA · PI FETHKE, NATHAN B · 2011 to 2025
$24.6M
CDC-NIOSH pilot grant 5 U54 OH007548NIOSH CDC HHS U54 OH007548
6 · The paper itself

Abstract

backgroundAnimal production workers are persistently exposed to organic dust and can suffer from a variety of respiratory disease symptoms and annual decline in lung function. The role of high mobility group box-1 (HMGB1) in inflammatory airway diseases is emerging. Hence, we tested a hypothesis that organic dust exposure of airway epithelial cells induces nucleocytoplasmic translocation of HMGB1 and blocking this translocation dampens organic dust-induced lung inflammation.

methodsRats were exposed to either ambient air or swine barn (8 h/day for either 1, 5, or 20 days) and lung tissues were processed for immunohistochemistry. Swine barn dust was collected and organic dust extract (ODE) was prepared and sterilized. Human airway epithelial cell line (BEAS-2B) was exposed to either media or organic dust extract followed by treatment with media or ethyl pyruvate (EP) or anti-HMGB1 antibody. Immunoblotting, ELISA and other assays were performed at 0 (control), 6, 24 and 48 h. Data (as mean ± SEM) was analyzed using one or two-way ANOVA followed by Bonferroni's post hoc comparison test. A p value of less than 0.05 was considered significant.

resultsCompared to controls, barn exposed rats showed an increase in the expression of HMGB1 in the lungs. Compared to controls, ODE exposed BEAS-2B cells showed nucleocytoplasmic translocation of HMGB1, co-localization of HMGB1 and RAGE, reactive species and pro-inflammatory cytokine production. EP treatment reduced the ODE induced nucleocytoplasmic translocation of HMGB1, HMGB1 expression in the cytoplasmic fraction, GM-CSF and IL-1β production and augmented the production of TGF-β1 and IL-10. Anti-HMGB1 treatment reduced ODE-induced NF-κB p65 expression, IL-6, ROS and RNS but augmented TGF-β1 and IL-10 levels.

conclusionsHMGB1-RAGE signaling is an attractive target to abrogate OD-induced lung inflammation.

Indexed as

DustActive Transport, Cell NucleusAnimalsCell LineCytokinesHMGB1 ProteinHumansImmunohistochemistryPneumoniaPyruvatesRatsReceptor for Advanced Glycation End ProductsRespiratory Tract DiseasesSignal TransductionSwineAger protein, ratCytokinesDustethyl pyruvateHbp1 protein, ratHMGB1 ProteinPyruvatesReceptor for Advanced Glycation End ProductsEthyl pyruvateHMGB1Lung inflammationOrganic dustRAGE

Identifiers

PMID30728013
PMCPMC6364446
OpenAlexW2913828105

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.