ArticleParticle and fibre toxicology2009
Pathway focused protein profiling indicates differential function for IL-1B, -18 and VEGF during initiation and resolution of lung inflammation evoked by carbon nanoparticle exposure in mice.
Article in Particle and fibre toxicology, 2009. 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, 39 citations in OpenAlex.
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- High expression of IL-1β and NFκB in tumor tissue predicts a low recurrence rate of hepatocellular carcinoma.International journal of clinical and experimental pathology · 2018Article
- Transcriptomic analysis comparing mouse strains with extreme total lung capacities identifies novel candidate genes for pulmonary function.Respiratory research · 2017Article
- Early pulmonary response is critical for extra-pulmonary carbon nanoparticle mediated effects: comparison of inhalation versus intra-arterial infusion exposures in mice.Particle and fibre toxicology · 2017Article
- Article
- Nanoparticle exposure reactivates latent herpesvirus and restores a signature of acute infection.Particle and fibre toxicology · 2017Article
- No involvement of alveolar macrophages in the initiation of carbon nanoparticle induced acute lung inflammation in mice.Particle and fibre toxicology · 2016Article
- Intracellular signal modulation by nanomaterials.Advances in experimental medicine and biology · 2014Review
- Comparison of particle-exposure triggered pulmonary and systemic inflammation in mice fed with three different diets.Particle and fibre toxicology · 2011Article
- Carbon-nanoparticle-triggered acute lung inflammation and its resolution are not altered in PPARγ-defective (P465L) mice.Particle and fibre toxicology · 2011Article
- Impaired resolution of inflammatory response in the lungs of JF1/Msf mice following carbon nanoparticle instillation.Respiratory research · 2011Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCarbonaceous nanoparticles possess an emerging source of human exposure due to the massive release of combustion products and the ongoing revolution in nanotechnology. Pulmonary inflammation caused by deposited nanoparticles is central for their adverse health effects. Epidemiological studies suggest that individuals with favourable lung physiology are at lower risk for particulate matter associated respiratory diseases probably due to efficient control of inflammation and repair process. Therefore we selected a mouse strain C3H/HeJ (C3) with robust lung physiology and exposed it to moderately toxic carbon nanoparticles (CNP) to study the elicited pulmonary inflammation and its resolution.
methods5 mug, 20 mug and 50 mug CNP were intratracheally (i.t.) instilled in C3 mice to identify the optimal dose for subsequent time course studies. Pulmonary inflammation was assessed using histology, bronchoalveolar lavage (BAL) analysis and by a panel of 62 protein markers.
results1 day after instillation of CNP, C3 mice exhibited a typical dose response, with the lowest dose (5 mug) representing the 'no effect level' as reflected by polymorphonuclear leucocyte (PMN), and BAL/lung concentrations of pro-inflammatory proteins. Histological analysis and BAL-protein concentration did not reveal any evidence of tissue injury in 20 mug CNP instilled animals. Accordingly time course assessment of the inflammatory response was performed after 3 and 7 days with this dose (20 mug). Compared to day 1, BAL PMN counts were significantly decreased at day 3 and completely returned to normal by day 7. We have identified protein markers related to the acute response and also to the time dependent response in lung and BAL. After complete resolution of PMN influx on day 7, we detected elevated concentrations of 20 markers that included IL1B, IL18, FGF2, EDN1, and VEGF in lung and/or BAL. Biological pathway analysis revealed these factors to be involved in a closely regulated molecular cascade with IL1B/IL18 as upstream and FGF2/EDN1/VEGF as downstream molecules.
conclusionConsidering the role of VEGF, FGF2 and EDN1 in lung development and morphogenesis together with the lack of any evident tissue damage we suggest a protective/homeostatic machinery to be associated in lungs of stable organisms to counter the CNP challenge as a precautionary measure.
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Registered trials
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