ArticlePloS one2014
Allergic airway inflammation by nasal inoculation of particulate matter (PM2.5) in NC/Nga mice.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 40 papers.
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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.
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Who cites it
40 citing papers in PubMed, 95 citations in OpenAlex.
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- NLRP3 inflammasome activation in response to metals.Frontiers in immunology · 2023Review
- Toxicological Effects of Fine Particulate Matter (PMWater, air, and soil pollution · 2023Review
- Article
- Interaction between the hypothalamo-pituitary-adrenal and thyroid axes during immobilization stress.Frontiers in physiology · 2022Article
- The Correlation of PM2.5 Exposure with Acute Attack and Steroid Sensitivity in Asthma.BioMed research international · 2022Review
- Immunoglobulin E-Dependent Activation of Immune Cells in Rhinovirus-Induced Asthma Exacerbation.Frontiers in allergy · 2022Article
- Loss of E-cadherin due to road dust PMEnvironmental science and pollution research international · 2021Article
- Particulate matter 2.5 triggers airway inflammation and bronchial hyperresponsiveness in mice by activating the SIRT2-p65 pathway.Frontiers of medicine · 2021Article
- YG-1 Extract Improves Acute Pulmonary Inflammation by Inducing Bronchodilation and Inhibiting Inflammatory Cytokines.Nutrients · 2021Article
- Fine particulate matter induces airway inflammation by disturbing the balance between Th1/Th2 and regulation of GATA3 and Runx3 expression in BALB/c mice.Molecular medicine reports · 2021Article
- Effects of Betulinic Acid Derivative on Lung Inflammation in a Mouse Model of Chronic Obstructive Pulmonary Disease Induced by Particulate Matter 2.5.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Airway hyperresponsiveness development and the toxicity of PM2.5.Environmental science and pollution research international · 2021Review
- PM2.5 Aggravated OVA-Induced Epithelial Tight Junction Disruption Through Fas Associated via Death Domain-Dependent Apoptosis in Asthmatic Mice.Journal of asthma and allergy · 2021Article
- Nrf2 mitigates prolonged PM2.5 exposure-triggered liver inflammation by positively regulating SIKE activity: Protection by Juglanin.Redox biology · 2020Article
- Long-term PMAging · 2020Article
- Nrf2 deficiency aggravates PMAging · 2020Article
- Pulmonary inflammation induced by low-dose particulate matter exposure in mice.American journal of physiology. Lung cellular and molecular physiology · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To evaluate the effect of airborne particulate matter 2.5 (PM2.5) in winter on airway inflammation, water-soluble supernatant (Sup) and water-insoluble precipitate (Pre) in PM2.5 were inoculated in NC/Nga mice with high sensitivity to mite allergens. Sup with aluminum oxide was injected intraperitoneally for sensitization. Five days later, Sup, Pre or both Sup and Pre were inoculated via the nasal route five times for more sensitization and a challenge inoculation on the 11th day in NC/Nga mice. On the 12th day, mice were examined for airway hyperresponsiveness (AHR), BALF cell count and IL-1β concentration, mRNA expression of Th1 and Th2 cytokines, chemokines such as eotaxin 1 and eotaxin 2, inflammasomal complex molecules such as IL-1β, caspase 1 and the nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) in lung tissue as well as histopathology. The synergistic effect of Sup and Pre was observed in terms of increases in AHR, BALF cells, the mRNA expression of IL-13, eotaxin1 and IL-1β, and the IL-1β concentration in BALF. Intracellular deposits of insoluble particulates were observed in macrophages around inflammatory granulation of the mouse group treated with Sup and Pre. These results suggest that PM2.5 can induce airway hyperresponsiveness in mice with genetically high sensitivity to mite allergens by an inflammasome-associated mechanism and synergistic action of insoluble particulates and soluble components.
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