ArticleeLife2015
Nanoparticulate carbon black in cigarette smoke induces DNA cleavage and Th17-mediated emphysema.
Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04918706 (An Explorative Study for Halting Inflammation in Patients With Emphysema by Administration of Allogeneic Bone Marrow Derived Mesenchymal Stromal Cells.), which is not on this 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.
An Explorative Study for Halting Inflammation in Patients With Emphysema by Administration of Allogeneic Bone Marrow Derived Mesenchymal Stromal Cells.
Who cites it
48 citing papers in PubMed, 86 citations in OpenAlex.
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- Heterogeneous impact of fine particulate matter constituents on pulmonary tuberculosis onset: a multicenter time series study in Beijing.BMC public health · 2025Article
- N6-methyladenosine-modified circDCP2 promotes carbon black nanoparticle-induced malignancy in human bronchial epithelial cells via PI3K-AKT pathway and macrophage homeostasis.Journal of nanobiotechnology · 2025Article
- Carbonaceous particle exposure triggered accumulation of Osteopontin/SPP1+ macrophages contributes to emphysema development.MedComm · 2025Article
- The cGAS-STING pathway in COPD: targeting its role and therapeutic potential.Respiratory research · 2024Review
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- Insights into the toxicological effects of nanomaterials on atherosclerosis: mechanisms involved and influence factors.Journal of nanobiotechnology · 2023Review
- Contribution of adaptive immunity to human COPD and experimental models of emphysema.Physiological reviews · 2023Review
- Chronic exposure to carbon black ultrafine particles reprograms macrophage metabolism and accelerates lung cancer.Science advances · 2022Article
- Black carbon content in airway macrophages is associated with increased severe exacerbations and worse COPD morbidity in SPIROMICS.Respiratory research · 2022Article
- Carbonaceous Nanoparticle Air Pollution: Toxicity and Detection in Biological Samples.Nanomaterials (Basel, Switzerland) · 2022Review
- Demystifying idiopathic interstitial pneumonia: time for more etiology-focused nomenclature in interstitial lung disease.Expert review of respiratory medicine · 2022Review
- Transient Ascaris suum larval migration induces intractable chronic pulmonary disease and anemia in mice.PLoS neglected tropical diseases · 2021Article
- Citrullinated vimentin mediates development and progression of lung fibrosis.Science translational medicine · 2021Article
- Human Lung Conventional Dendritic Cells Orchestrate Lymphoid Neogenesis during Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Chronic inhalation of cigarette smoke is the major cause of sterile inflammation and pulmonary emphysema. The effect of carbon black (CB), a universal constituent of smoke derived from the incomplete combustion of organic material, in smokers and non-smokers is less known. In this study, we show that insoluble nanoparticulate carbon black (nCB) accumulates in human myeloid dendritic cells (mDCs) from emphysematous lung and in CD11c(+) lung antigen presenting cells (APC) of mice exposed to smoke. Likewise, nCB intranasal administration induced emphysema in mouse lungs. Delivered by smoking or intranasally, nCB persisted indefinitely in mouse lung, activated lung APCs, and promoted T helper 17 cell differentiation through double-stranded DNA break (DSB) and ASC-mediated inflammasome assembly in phagocytes. Increasing the polarity or size of CB mitigated many adverse effects. Thus, nCB causes sterile inflammation, DSB, and emphysema and explains adverse health outcomes seen in smokers while implicating the dangers of nCB exposure in non-smokers.
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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.