Evidence map›Paper›PMID 39992237›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2025

Mast cells are key mediators in the pulmonary inflammatory response to formaldehyde exposure.

Matthew Gibb, Angela N Reinert, Troy Schedin, Daniel T Merrick, Jared M Brown, Alison K Bauer

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

6 authors.

Matthew GibbDepartment of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, United States.
Angela N ReinertDepartment of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, United States.
Troy SchedinDepartment of Immunology and Microbiology, Human Immune Monitoring Shared Resource, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, United States.
Daniel T MerrickDepartment of Pathology, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, United States.
Jared M BrownDepartment of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, United States.
Alison K BauerDepartment of Environmental and Occupational Health, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, United States.ORCID 0000-0003-4477-9899

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Training in Molecular and Systems ToxicologyT32ES029074 · NIEHS · UNIVERSITY OF COLORADO DENVER · PI Jared Michael Brown · 2019 to 2026
$1.1M
Mast Cell Activation as a Common Mechanism of Pulmonary Toxicity by Chemical Threat AgentsR56ES034386 · NIEHS · UNIVERSITY OF COLORADO DENVER · PI BAUER, ALISON K, BROWN, JARED MICHAEL · 2023 to 2023
$463k
NCI NIH HHS P30 CA046934NIEHS NIH HHS R56 ES034386NIEHS NIH HHS R56ES034386NIEHS NIH HHS T32 ES029074NIH HHSUniversity of Colorado Cancer Center P30CA046934
6 · The paper itself

Abstract

Formaldehyde (FA) is a common chemical linked to respiratory problems such as airway hyperresponsiveness and pulmonary inflammation. Due to its toxicological effects and ease of mass production, FA is also recognized as a significant chemical threat by the U.S. Department of Homeland Security. This study investigates the role of mast cells in the pulmonary inflammatory response to acute high-dose FA exposure. Using wild-type (C57BL/6J) and mast cell-deficient (KitW-sh) mouse models, we assessed the impact of oropharyngeal aspiration of FA on lung pathology. Our findings reveal that C57BL/6J mice experienced significant increases in cellular infiltration, altered immune cell populations, and changes in lipid mediator profiles. In contrast, KitW-sh mice exhibited significantly reduced inflammatory responses. Notably, the presence of mast cells was associated with enhanced dendritic cell migration and differential production of bioactive lipid mediators, such as specialized pro-resolving mediators and pro-inflammatory leukotrienes in C57BL/6J mice. These results highlight the crucial role of mast cells in the immune response to FA and suggest they could be therapeutic targets for treating FA-induced lung inflammation.

Indexed as

FormaldehydeInflammation MediatorsLungMast CellsPneumoniaAnimalsBronchoalveolar Lavage FluidCell MovementDendritic CellsMaleMiceMice, Inbred C57BLFormaldehydeInflammation Mediatorschemical threat agentsdendritic cellformaldehydeinflammationinhalation exposuremast cell

Identifiers

PMID39992237
PMCPMC12038249

What OpenQuestion holds

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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.