ArticleToxicology and applied pharmacology2015
MyD88 mediates in vivo effector functions of alveolar macrophages in acute lung inflammatory responses to carbon nanotube exposure.
Article in Toxicology and applied pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Alveolar macrophages initiate the spatially targeted recruitment of neutrophils after nanoparticle inhalation.Science advances · 2025Article
- Carbon-based Nanomaterials in Photothermal Therapy Guided by Photoacoustic Imaging: State of Knowledge and Recent Advances.Current medicinal chemistry · 2025Review
- Carbon Nanotube Immunotoxicity in Alveolar Epithelial Type II Cells Is Mediated by Physical Contact-Independent Cell-Cell Interaction with Macrophages as Demonstrated in an Optimized Air-Liquid Interface (ALI) Coculture Model.Nanomaterials (Basel, Switzerland) · 2024Article
- Oro-Respiratory Dysbiosis and Its Modulatory Effect on Lung Mucosal Toxicity during Exposure or Co-Exposure to Carbon Nanotubes and Cigarette Smoke.Nanomaterials (Basel, Switzerland) · 2024Article
- Differential modulation of lung aquaporins among other pathophysiological markers in acute (ClFrontiers in physiology · 2022Article
- Microenvironmental Alterations in Carbon Nanotube-Induced Lung Inflammation and Fibrosis.Frontiers in cell and developmental biology · 2020Review
- Signaling Pathways Implicated in Carbon Nanotube-Induced Lung Inflammation.Frontiers in immunology · 2020Review
- Cellular Toxicity and Immunological Effects of Carbon-based Nanomaterials.Particle and fibre toxicology · 2019Review
- Role of Macrophages in Acute Lung Injury and Chronic Fibrosis Induced by Pulmonary Toxicants.Toxicological sciences : an official journal of the Society of Toxicology · 2019Review
- Air pollutants and early origins of respiratory diseases.Chronic diseases and translational medicine · 2018Article
- Macrophage sensing of single-walled carbon nanotubes via Toll-like receptors.Scientific reports · 2018Article
- Genetic susceptibility to toxicologic lung responses among inbred mouse strains following exposure to carbon nanotubes and profiling of underlying gene networks.Toxicology and applied pharmacology · 2017Article
- Seawater-drowning-induced acute lung injury: From molecular mechanisms to potential treatments.Experimental and therapeutic medicine · 2017Article
- Early signs of multi-walled carbon nanotbues degradation in macrophages, via an intracellular pH-dependent biological mechanism; importance of length and functionalization.Particle and fibre toxicology · 2016Article
- Myofibroblasts and lung fibrosis induced by carbon nanotube exposure.Particle and fibre toxicology · 2016Review
- Potential of PEGylated Toll-Like Receptor 7 Ligands for Controlling Inflammation and Functional Changes in Mouse Models of Asthma and Silicosis.Frontiers in immunology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Carbon nanotubes (CNTs) are rapidly emerging as high-priority occupational toxicants. CNT powders contain fibrous particles that aerosolize readily in places of manufacture and handling, posing an inhalation risk for workers. Studies using animal models indicate that lung exposure to CNTs causes prolonged inflammatory responses and diffuse alveolar injury. The mechanisms governing CNT-induced lung inflammation are not fully understood but have been suggested to involve alveolar macrophages (AMs). In the current study, we sought to systematically assess the effector role of AMs in vivo in the induction of lung inflammatory responses to CNT exposures and investigate their cell type-specific mechanisms. Multi-wall CNTs characterized for various physicochemical attributes were used as the CNT type. Using an AM-specific depletion and repopulation approach in a mouse model, we unambiguously demonstrated that AMs are major effector cells necessary for the in vivo elaboration of CNT-induced lung inflammation. We further investigated in vitro AM responses and identified molecular targets which proved critical to pro-inflammatory responses in this model, namely MyD88 as well as MAPKs and Ca(2+)/CamKII. We further demonstrated that MyD88 inhibition in donor AMs abrogated their capacity to reconstitute CNT-induced inflammation when adoptively transferred into AM-depleted mice. Taken together, this is the first in vivo demonstration that AMs act as critical effector cell types in CNT-induced lung inflammation and that MyD88 is required for this in vivo effector function. AMs and their cell type-specific mechanisms may therefore represent potential targets for future therapeutic intervention of CNT-related lung injury.
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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.