ArticleToxicological sciences : an official journal of the Society of Toxicology2018
Specialized Pro-Resolving Lipid Mediators Regulate Ozone-Induced Pulmonary and Systemic Inflammation.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 65 citations in OpenAlex.
- EPA-Derived Oxylipin Incorporation into Tissues of High-Fat Diet-Fed Mice and Its Consequences for n-6 PUFA-Derived Oxylipins.The Journal of nutrition · 2026Article
- CD163 protects against pulmonary injury and inflammation induced by acute ObioRxiv : the preprint server for biology · 2026Article
- Resolvin D1 requires TLR2-FPR2 crosstalk for inflammation resolution and protection during ocular bacterial infection.Communications biology · 2026Article
- Pro-resolving lipid mediators in diseases: exploring the molecular basis and clinical implication.Molecular biomedicine · 2026Review
- Docosahexaenoic Acid and Its Metabolites Protect against Ozone-induced Pulmonary Inflammation.American journal of respiratory cell and molecular biology · 2025Article
- Article
- ALX/FPR2 Contributes to Serum Amyloid A-Induced Lung Neutrophil Recruitment Following Acute Ozone Exposure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Ozone-Induced Lung Injury are Mediated Via PPAR-Mediated Ferroptosis in Mice.Biological trace element research · 2025Article
- Mast cells are key mediators in the pulmonary inflammatory response to formaldehyde exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Article
- Emerging mechanisms of organ crosstalk: The role of oxylipins.Nutrition bulletin · 2025Review
- Dietary Eicosapentaenoic Acid Improves Ozone-Induced Pulmonary Inflammation in C57BL/6 Mice.The Journal of nutrition · 2025Article
- Associations between omega-3 fatty acid-derived lipid mediators and markers of inflammation in older subjects with low-grade chronic inflammation.Prostaglandins & other lipid mediators · 2025Article
- Specialized Pro-Resolving Lipid Mediators Distinctly Modulate Silver Nanoparticle-Induced Pulmonary Inflammation in Healthy and Metabolic Syndrome Mouse Models.Nanomaterials (Basel, Switzerland) · 2024Article
- Molecular changes underlying pulmonary emphysema and chronic bronchitis in Chronic Obstructive Pulmonary Disease: An updated review.Histology and histopathology · 2024Review
- Neuroinflammation is dependent on sex and ovarian hormone presence following acute woodsmoke exposure.Scientific reports · 2024Article
- Inconsequential role for chemerin-like receptor 1 in the manifestation of ozone-induced lung pathophysiology in male mice.Physiological reports · 2024Article
- Lipid mediators of inhalation exposure-induced pulmonary toxicity and inflammation.Inhalation toxicology · 2024Review
- Exploring the influence of environmental indicators and forecasting influenza incidence using ARIMAX models.Frontiers in public health · 2024Article
- Mechanisms of ozone-induced neurotoxicity in the development and progression of dementia: a brief review.Frontiers in aging neuroscience · 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
15 authors at 4 institutions in 1 country.
Funding
Abstract
Exposure to ozone (O3) induces lung injury, pulmonary inflammation, and alters lipid metabolism. During tissue inflammation, specialized pro-resolving lipid mediators (SPMs) facilitate the resolution of inflammation. SPMs regulate the pulmonary immune response during infection and allergic asthma; however, the role of SPMs in O3-induced pulmonary injury and inflammation is unknown. We hypothesize that O3 exposure induces pulmonary inflammation by reducing SPMs. To evaluate this, male C57Bl/6J mice were exposed to filtered air (FA) or 1 ppm O3 for 3 h and necropsied 24 h after exposure. Pulmonary injury/inflammation was determined by bronchoalveolar lavage (BAL) differentials, protein, and lung tissue cytokine expression. SPMs were quantified by liquid chromatography tandem mass spectrometry and SPM receptors leukotriene B4 receptor 1 (BLT-1), formyl peptide receptor 2 (ALX/FPR2), chemokine-like receptor 1 (ChemR23), and SPM-generating enzyme (5-LOX and 12/15-LOX) expression were measured by real time PCR. 24 h post-O3 exposure, BAL PMNs and protein content were significantly increased compared to FA controls. O3-induced lung inflammation was associated with significant decreases in pulmonary SPM precursors (14-HDHA, 17-HDHA), the SPM PDX, and in pulmonary ALX/FPR2, ChemR23, and 12/15-LOX expression. Exogenous administration of 14-HDHA, 17-HDHA, and PDX 1 h prior to O3 exposure rescued pulmonary SPM precursors/SPMs, decreased proinflammatory cytokine and chemokine expression, and decreased BAL macrophages and PMNs. Taken together, these data indicate that O3-mediated SPM reductions may drive O3-induced pulmonary inflammation.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.