ReviewBMJ open respiratory research2023
Chemical exposure and alveolar macrophages responses: 'the role of pulmonary defense mechanism in inhalation injuries'.
Review in BMJ open respiratory research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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.
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.
Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Environmentally relevant aged nanoplastics amplify oxidative stress-associated inhalation toxicity and delay lung clearance.Redox biology · 2026Article
- Pharmacological Insights intoMolecules (Basel, Switzerland) · 2026Review
- Defined culture conditions improve functional properties of mature iPSC-derived macrophages for therapeutic screening.Stem cell research & therapy · 2026Article
- Lung injury, oxidative stress, and impaired functioning in a model of prolonged ozone exposure in female mice are associated with macrophage proinflammatory and profibrotic activation and altered bioenergetics.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Reactive Oxygen Species in Asthma: Regulators of Macrophage Polarization and Therapeutic Implications: A Narrative Review.Journal of asthma and allergy · 2025Review
- Review
- Artisanal Gem Mining in Brazil: Evaluation of Oxidative Stress and Genotoxicity Biomarkers.International journal of environmental research and public health · 2024Article
- Differential pulmonary toxicity and autoantibody formation in genetically distinct mouse strains following combined exposure to silica and diesel exhaust particles.Particle and fibre toxicology · 2024Article
- Epigenetic mechanisms of alveolar macrophage activation in chemical-induced acute lung injury.Frontiers in immunology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidemiological and clinical studies have indicated an association between particulate matter (PM) exposure and acute and chronic pulmonary inflammation, which may be registered as increased mortality and morbidity. Despite the increasing evidence, the pathophysiology mechanism of these PMs is still not fully characterised. Pulmonary alveolar macrophages (PAMs), as a predominant cell in the lung, play a critically important role in these pathological mechanisms. Toxin exposure triggers events associated with macrophage activation, including oxidative stress, acute damage, tissue disruption, remodelling and fibrosis. Targeting macrophage may potentially be employed to treat these types of lung inflammation without affecting the natural immune response to bacterial infections. Biological toxins, their sources of exposure, physical and other properties, and their effects on the individuals are summarised in this article. Inhaled particulates from air pollution and toxic gases containing chemicals can interact with alveolar epithelial cells and immune cells in the airways. PAMs can sense ambient pollutants and be stimulated, triggering cellular signalling pathways. These cells are highly adaptable and can change their function and phenotype in response to inhaled agents. PAMs also have the ability to polarise and undergo plasticity in response to tissue damage, while maintaining resistance to exposure to inhaled agents.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.