Evidence map›Paper›PMID 36538286›Full record

ArticleJournal of immunotoxicology2023

Effect of epithelial-specific MyD88 signaling pathway on airway inflammatory response to organic dust exposure.

Amber N Johnson, John Dickinson, Amy Nelson, Rohit Gaurav, Katrina Kudrna, Scott E Evans, Katherine Janike, Todd A Wyatt, Jill A Poole

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

Article in Journal of immunotoxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

5 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Respiratory Diseases Associated With Organic Dust Exposure.The journal of allergy and clinical immunology. In practice · 2024
    Review
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

9 authors at 3 institutions in 1 country.

Amber N JohnsonDepartment of Internal Medicine, Pulmonary Critical Care and Sleep Division, University of Nebraska Medical Center (UNMC), Omaha, NE, USA.
John DickinsonDepartment of Internal Medicine, Pulmonary Critical Care and Sleep Division, University of Nebraska Medical Center (UNMC), Omaha, NE, USA.
Amy NelsonDepartment of Internal Medicine, Allergy and Immunology Division, University of Nebraska Medical Center (UNMC), Omaha, NE, USA.
Rohit GauravDepartment of Internal Medicine, Allergy and Immunology Division, University of Nebraska Medical Center (UNMC), Omaha, NE, USA.ORCID 0000-0003-4753-2680
Katrina KudrnaDepartment of Internal Medicine, Pulmonary Critical Care and Sleep Division, University of Nebraska Medical Center (UNMC), Omaha, NE, USA.
Scott E EvansDepartment of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Katherine JanikeDepartment of Internal Medicine, Allergy and Immunology Division, University of Nebraska Medical Center (UNMC), Omaha, NE, USA.
Todd A WyattDepartment of Internal Medicine, Pulmonary Critical Care and Sleep Division, University of Nebraska Medical Center (UNMC), Omaha, NE, USA.ORCID 0000-0002-9273-6730
Jill A PooleDepartment of Internal Medicine, Allergy and Immunology Division, University of Nebraska Medical Center (UNMC), Omaha, NE, USA.
University of Nebraska Medical Center · USNebraska Medical Center · USThe University of Texas MD Anderson Cancer Center · US

Funding

UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI James Eudy · 1985 to 2026
$55.0M
Surveillance of Agricultural Injuries in the Central States RegionsU54OH010162 · OH · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI RAUTIAINEN, RISTO HEIKKI · 2011 to 2025
$23.6M
Inducible epithelial resistance: a program investigating mechanisms to protect against acute and chronic complications of pneumoniaR35HL144805 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI EVANS, SCOTT E. · 2019 to 2025
$6.2M
Role of pattern recognition receptors in organic dust-induced airway inflammationR01ES019325 · NIEHS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI POOLE, JILL A · 2010 to 2020
$3.7M
Autophagy-mediated mucin degradation is necessary for resolution of mucous metaplasiaR01HL157269 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI DICKINSON, JOHN DAVID · 2021 to 2025
$2.7M
Resolving Occupational Exposure-Induced Lung DiseaseR01OH012045 · OH · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI POOLE, JILL A · 2021 to 2024
$2.3M
BLRD VA IK6 BX005962NCI NIH HHS P30 CA036727NHLBI NIH HHS R01 HL157269NHLBI NIH HHS R35 HL144805NIEHS NIH HHS R01 ES019325NIOSH CDC HHS R01 OH012045NIOSH CDC HHS U54 OH010162
6 · The paper itself

Abstract

The Toll-like receptor (TLR) adaptor protein MyD88 is integral to airway inflammatory response to microbial-enriched organic dust extract (ODE) exposures. ODE-induced airway neutrophil influx and release of pro-inflammatory cytokines was essentially abrogated in global MyD88-deficient mice, yet these mice demonstrate an increase in airway epithelial cell mucin expression. To further elucidate the role of MyD88-dependent responses specific to lung airway epithelial cells in response to ODE

Indexed as

Inhalation ExposureMyeloid Differentiation Factor 88AnimalsDustInterleukin-6MiceMice, Inbred C57BLMucinsSignal TransductionToll-Like ReceptorsTumor Necrosis Factor-alphaDustInterleukin-6MucinsMyd88 protein, mouseMyeloid Differentiation Factor 88Toll-Like ReceptorsTumor Necrosis Factor-alphaadaptationagricultureairway inflammationEnvironmental respiratory diseaseMyD88occupationalorganic dust

Identifiers

PMID36538286
PMCPMC9912912
OpenAlexW4312095710

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.