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High concentrations of Printex 90 carbon black ultrafine particles disturb the epithelial barrier in human primary respiratory mucosa models.

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Title: High concentrations of Printex 90 carbon black ultrafine particles disturb the epithelial barrier in human primary respiratory mucosa models.
Authors: Ehret Kasemo, Totta1 (AUTHOR) ehret_t@ukw.de, Oppmann, Maximilian2 (AUTHOR), Dembski, Sofia2 (AUTHOR), Steinke, Maria1 (AUTHOR), Lajtha, Elena1 (AUTHOR), Moratin, Helena1 (AUTHOR), Stöth, Manuel1 (AUTHOR), Scherzad, Agmal1 (AUTHOR), Delaval, Mathilde Noémie3 (AUTHOR), Zimmermann, Ralf3,4 (AUTHOR), Di Bucchianico, Sebastiano3,4 (AUTHOR), Hackenberg, Stephan1 (AUTHOR), Meyer, Till J.1 (AUTHOR)
Source: Environmental Toxicology & Pharmacology. Oct2025, Vol. 119, pN.PAG-N.PAG. 1p.
Subject Terms: *Carbon-black, Respiratory mucosa, DNA damage, Cell adhesion, Cell junctions, Mucociliary system, Nanoparticles, Cytotoxins
Abstract: Airborne pollutants harm human health, but the mechanisms involved remain unclear. Impaired epithelial barrier function is, as in respiratory diseases, one possible pathomechanism. To investigate this, carbon black (CB) as a model for ultrafine particles (UFP), was applied to respiratory mucosa models of primary fibroblasts and epithelial cells cultured at the air-liquid interface (ALI). Models were assessed for the mucociliary phenotype. Cytotoxicity, DNA damage, and barrier integrity were evaluated by the lactate dehydrogenase (LDH) and comet assays, and by transepithelial electrical resistance (TEER) measurements. Cilia movement and ultrastructure, secretory cells, and intact cell-cell contacts were confirmed. Subtle changes were observed: the LDH release had increased 2 h post exposure and barrier disturbance 24 h post exposure was detected, both without mucosal damage or genotoxic effects. Donor-specific differences were present. Barrier disruption without cell detachment or death suggests model feasibility for long-term studies of, e.g. , tissue regeneration or fibrosis following UFP exposure. [Display omitted] • Human upper respiratory system mucosal model with high in vivo -correlation. • Ultrafine particle exposures at the air-liquid interface. • Subtle responses are consistent with minor acute effects in epidemiological data. • Minor effects enable future UFP exposures to study regeneration or fibrosis. [ABSTRACT FROM AUTHOR]
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Database: GreenFILE
Description
Abstract:Airborne pollutants harm human health, but the mechanisms involved remain unclear. Impaired epithelial barrier function is, as in respiratory diseases, one possible pathomechanism. To investigate this, carbon black (CB) as a model for ultrafine particles (UFP), was applied to respiratory mucosa models of primary fibroblasts and epithelial cells cultured at the air-liquid interface (ALI). Models were assessed for the mucociliary phenotype. Cytotoxicity, DNA damage, and barrier integrity were evaluated by the lactate dehydrogenase (LDH) and comet assays, and by transepithelial electrical resistance (TEER) measurements. Cilia movement and ultrastructure, secretory cells, and intact cell-cell contacts were confirmed. Subtle changes were observed: the LDH release had increased 2 h post exposure and barrier disturbance 24 h post exposure was detected, both without mucosal damage or genotoxic effects. Donor-specific differences were present. Barrier disruption without cell detachment or death suggests model feasibility for long-term studies of, e.g. , tissue regeneration or fibrosis following UFP exposure. [Display omitted] • Human upper respiratory system mucosal model with high in vivo -correlation. • Ultrafine particle exposures at the air-liquid interface. • Subtle responses are consistent with minor acute effects in epidemiological data. • Minor effects enable future UFP exposures to study regeneration or fibrosis. [ABSTRACT FROM AUTHOR]
ISSN:13826689
DOI:10.1016/j.etap.2025.104829