ArticleParticle and fibre toxicology2021
Nanomaterial- and shape-dependency of TLR2 and TLR4 mediated signaling following pulmonary exposure to carbonaceous nanomaterials in mice.
Article in Particle and fibre toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 59 citations in OpenAlex.
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- Toward a ToxAtlas of Carbon-Based Nanomaterials: Single-Cell RNA Sequencing Reveals Initiating Cell Circuits in Pulmonary Inflammation.ACS nano · 2025Article
- Alveolar macrophages initiate the spatially targeted recruitment of neutrophils after nanoparticle inhalation.Science advances · 2025Article
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- Intratracheal instillation of graphene oxide with different diameters suppressed toll-like receptor 3-mediated lipid droplet biogenesis in lungs and livers of mice.Toxicology research · 2025Article
- Exploring 2D Graphene-Based Nanomaterials for Biomedical Applications: A Theoretical Modeling Perspective.Small science · 2025Article
- Lung epithelial and alveolar macrophage-like cell interactions significantly modify innate responses to bacterial endotoxin with the involvement of direct cellular contacts, TNF-α, ICAM1 and MCP-1.Frontiers in immunology · 2025Article
- Oxide-Perovskites for Automotive Catalysts Biotransform and Induce Multicomponent Clearance and Hazard.ACS nano · 2024Article
- Pulmonary toxicity assessment of polypropylene, polystyrene, and polyethylene microplastic fragments in mice.Toxicological research · 2024Article
- Environmental and Health Impacts of Graphene and Other Two-Dimensional Materials: A Graphene Flagship Perspective.ACS nano · 2024Review
- Distinct Pro-Inflammatory Mechanisms Elicited by Short and Long Amosite Asbestos Fibers in Macrophages.International journal of molecular sciences · 2023Article
- Comparing the Toxicological Responses of Pulmonary Air-Liquid Interface Models upon Exposure to Differentially Treated Carbon Fibers.International journal of molecular sciences · 2023Article
- Acute phase response following pulmonary exposure to soluble and insoluble metal oxide nanomaterials in mice.Particle and fibre toxicology · 2023Article
- Inflammatory Genes Associated with Pristine Multi-Walled Carbon Nanotubes-Induced Toxicity in Ocular Cells.International journal of nanomedicine · 2023Article
- Understanding the immunological interactions of engineered nanomaterials: Role of the bio-corona.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2022Review
- Passage of exogeneous fine particles from the lung into the brain in humans and animals.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Characterization of ENM Dynamic Dose-Dependent MOA in Lung with Respect to Immune Cells Infiltration.Nanomaterials (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPulmonary exposure to high doses of engineered carbonaceous nanomaterials (NMs) is known to trigger inflammation in the lungs paralleled by an acute phase response. Toll-like receptors (TLRs), particularly TLR2 and TLR4, have recently been discussed as potential NM-sensors, initiating inflammation. Using Tlr2 and Tlr4 knock out (KO) mice, we addressed this hypothesis and compared the pattern of inflammation in lung and acute phase response in lung and liver 24 h after intratracheal instillation of three differently shaped carbonaceous NMs, spherical carbon black (CB), multi-walled carbon nanotubes (CNT), graphene oxide (GO) plates and bacterial lipopolysaccharide (LPS) as positive control.
resultsThe LPS control confirmed a distinct TLR4-dependency as well as a pronounced contribution of TLR2 by reducing the levels of pulmonary inflammation to 30 and 60% of levels in wild type (WT) mice. At the doses chosen, all NM caused comparable neutrophil influxes into the lungs of WT mice, and reduced levels were only detected for GO-exposed Tlr2 KO mice (35%) and for CNT-exposed Tlr4 KO mice (65%). LPS-induced gene expression was strongly TLR4-dependent. CB-induced gene expression was unaffected by TLR status. Both GO and MWCNT-induced Saa1 expression was TLR4-dependent. GO-induced expression of Cxcl2, Cxcl5, Saa1 and Saa3 were TLR2-dependent. NM-mediated hepatic acute phase response in terms of liver gene expression of Saa1 and Lcn2 was shown to depend on TLR2 for all three NMs. TLR4, in contrast, was only relevant for the acute phase response caused by CNTs, and as expected by LPS.
conclusionTLR2 and TLR4 signaling was not involved in the acute inflammatory response caused by CB exposure, but contributed considerably to that of GO and CNTs, respectively. The strong involvement of TLR2 in the hepatic acute phase response caused by pulmonary exposure to all three NMs deserves further investigations.
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