ArticleParticle and fibre toxicology2014
The alarmin IL-1α is a master cytokine in acute lung inflammation induced by silica micro- and nanoparticles.
Article in Particle and fibre toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 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
79 citing papers in PubMed, 165 citations in OpenAlex.
- Electric Field-Induced Release and Measurement Liquid Biopsy of Urinary Transcriptomics and Key Proteins from Normal and High-risk Pregnant Women.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Alignment of in vitro and in vivo pulmonary inflammation models using crystalline quartz silica.Particle and fibre toxicology · 2026Article
- Seasonal Variation in PMAntioxidants (Basel, Switzerland) · 2026Article
- Autologous human iPSC-derived alveolus-on-chip reveals early pathological events ofScience advances · 2026Article
- Neutrophil-macrophage crosstalk network in acute lung injury: feedback circuits linking cytokine storm and cell death.Frontiers in cellular and infection microbiology · 2026Review
- Toward a ToxAtlas of Carbon-Based Nanomaterials: Single-Cell RNA Sequencing Reveals Initiating Cell Circuits in Pulmonary Inflammation.ACS nano · 2025Article
- Silicon Carbide Nanowires Impair Mucociliary Clearance-Mediated Innate Immunity in Primary Human Bronchial Epithelial Cells.ACS nano · 2025Article
- NLRP3 deficiency abrogates silica-induced neutrophil infiltration, pulmonary damage and fibrosis.Respiratory research · 2025Article
- Pulmonary exposure to renewable diesel exhaust particles alters protein expression and toxicity profiles in bronchoalveolar lavage fluid and plasma of mice.Archives of toxicology · 2025Article
- Interleukin-1 signaling and CD4Frontiers in immunology · 2025Article
- Short- and long-term pathologic responses to quartz are induced by nearly free silanols formed during crystal fracturing.Particle and fibre toxicology · 2024Article
- Exposure to bacterial PAMPs before RSV infection exacerbates innate inflammation and disease via IL-1α and TNF-α.Mucosal immunology · 2024Article
- Lung Single-Cell Transcriptomics Offers Insights into the Pulmonary Interstitial Toxicity Caused by Silica Nanoparticles.Environment & health (Washington, D.C.) · 2024Article
- Bi-directional regulation between inflammation and stem cells in the respiratory tract.Journal of cell science · 2024Review
- Air Pollution Drives Macrophage Senescence through a Phagolysosome-15-Lipoxygenase Pathway.ImmunoHorizons · 2024Article
- IL-1α is required for T cell-driven weight loss after respiratory viral infection.Mucosal immunology · 2024Article
- In vitro inflammation and toxicity assessment of pre- and post-incinerated organomodified nanoclays to macrophages using high-throughput screening approaches.Particle and fibre toxicology · 2024Article
- Air pollution drives macrophage senescence through a phagolysosome-15-lipoxygenase pathway.bioRxiv : the preprint server for biology · 2024Article
- Fungal chitin-binding glycoprotein induces Dectin-2-mediated allergic airway inflammation synergistically with chitin.PLoS pathogens · 2024Article
- The role of inflammation in silicosis.Frontiers in pharmacology · 2024Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInflammasome-activated IL-1β plays a major role in lung neutrophilic inflammation induced by inhaled silica. However, the exact mechanisms that contribute to the initial production of precursor IL-1β (pro-IL-1β) are still unclear. Here, we assessed the implication of alarmins (IL-1α, IL-33 and HMGB1) in the lung response to silica particles and found that IL-1α is a master cytokine that regulates IL-1β expression.
methodsPro- and mature IL-1β as well as alarmins were assessed by ELISA, Western Blot or qRT-PCR in macrophage cultures and in mouse lung following nano- and micrometric silica exposure. Implication of these immune mediators in the establishment of lung inflammatory responses to silica was investigated in knock-out mice or after antibody blockade by evaluating pulmonary neutrophil counts, CXCR2 expression and degree of histological injury.
resultsWe found that the early release of IL-1α and IL-33, but not HMGB1 in alveolar space preceded the lung expression of pro-IL-1β and neutrophilic inflammation in silica-treated mice. In vitro, the production of pro-IL-1β by alveolar macrophages was significantly induced by recombinant IL-1α but not by IL-33. Neutralization or deletion of IL-1α reduced IL-1β production and neutrophil accumulation after silica in mice. Finally, IL-1α released by J774 macrophages after in vitro exposure to a range of micro- and nanoparticles of silica was correlated with the degree of lung inflammation induced in vivo by these particles.
conclusionsWe demonstrated that in response to silica exposure, IL-1α is rapidly released from pre-existing stocks in alveolar macrophages and promotes subsequent lung inflammation through the stimulation of IL-1β production. Moreover, we demonstrated that in vitro IL-1α release from macrophages can be used to predict the acute inflammogenic activity of silica micro- and nanoparticles.
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.