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. |
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| 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] |
| Copyright of Environmental Toxicology & Pharmacology is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Database: | GreenFILE |
| FullText | Text: Availability: 0 |
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| Header | DbId: 8gh DbLabel: GreenFILE An: 188570892 AccessLevel: 6 PubType: Academic Journal PubTypeId: academicJournal PreciseRelevancyScore: 0 |
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| Items | – Name: Title Label: Title Group: Ti Data: High concentrations of Printex 90 carbon black ultrafine particles disturb the epithelial barrier in human primary respiratory mucosa models. – Name: Author Label: Authors Group: Au Data: <searchLink fieldCode="AR" term="%22Ehret+Kasemo%2C+Totta%22">Ehret Kasemo, Totta</searchLink><relatesTo>1</relatesTo> (AUTHOR)<i> ehret_t@ukw.de</i><br /><searchLink fieldCode="AR" term="%22Oppmann%2C+Maximilian%22">Oppmann, Maximilian</searchLink><relatesTo>2</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Dembski%2C+Sofia%22">Dembski, Sofia</searchLink><relatesTo>2</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Steinke%2C+Maria%22">Steinke, Maria</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Lajtha%2C+Elena%22">Lajtha, Elena</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Moratin%2C+Helena%22">Moratin, Helena</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Stöth%2C+Manuel%22">Stöth, Manuel</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Scherzad%2C+Agmal%22">Scherzad, Agmal</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Delaval%2C+Mathilde+Noémie%22">Delaval, Mathilde Noémie</searchLink><relatesTo>3</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Zimmermann%2C+Ralf%22">Zimmermann, Ralf</searchLink><relatesTo>3,4</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Di+Bucchianico%2C+Sebastiano%22">Di Bucchianico, Sebastiano</searchLink><relatesTo>3,4</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Hackenberg%2C+Stephan%22">Hackenberg, Stephan</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Meyer%2C+Till+J%2E%22">Meyer, Till J.</searchLink><relatesTo>1</relatesTo> (AUTHOR) – Name: TitleSource Label: Source Group: Src Data: <searchLink fieldCode="JN" term="%22Environmental+Toxicology+%26+Pharmacology%22">Environmental Toxicology & Pharmacology</searchLink>. Oct2025, Vol. 119, pN.PAG-N.PAG. 1p. – Name: Subject Label: Subject Terms Group: Su Data: *<searchLink fieldCode="DE" term="%22Carbon-black%22">Carbon-black</searchLink><br /><searchLink fieldCode="DE" term="%22Respiratory+mucosa%22">Respiratory mucosa</searchLink><br /><searchLink fieldCode="DE" term="%22DNA+damage%22">DNA damage</searchLink><br /><searchLink fieldCode="DE" term="%22Cell+adhesion%22">Cell adhesion</searchLink><br /><searchLink fieldCode="DE" term="%22Cell+junctions%22">Cell junctions</searchLink><br /><searchLink fieldCode="DE" term="%22Mucociliary+system%22">Mucociliary system</searchLink><br /><searchLink fieldCode="DE" term="%22Nanoparticles%22">Nanoparticles</searchLink><br /><searchLink fieldCode="DE" term="%22Cytotoxins%22">Cytotoxins</searchLink> – Name: Abstract Label: Abstract Group: Ab Data: 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] – Name: AbstractSuppliedCopyright Label: Group: Ab Data: <i>Copyright of Environmental Toxicology & Pharmacology is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.) |
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| RecordInfo | BibRecord: BibEntity: Identifiers: – Type: doi Value: 10.1016/j.etap.2025.104829 Languages: – Code: eng Text: English PhysicalDescription: Pagination: PageCount: 1 StartPage: N.PAG Subjects: – SubjectFull: Carbon-black Type: general – SubjectFull: Respiratory mucosa Type: general – SubjectFull: DNA damage Type: general – SubjectFull: Cell adhesion Type: general – SubjectFull: Cell junctions Type: general – SubjectFull: Mucociliary system Type: general – SubjectFull: Nanoparticles Type: general – SubjectFull: Cytotoxins Type: general Titles: – TitleFull: High concentrations of Printex 90 carbon black ultrafine particles disturb the epithelial barrier in human primary respiratory mucosa models. Type: main BibRelationships: HasContributorRelationships: – PersonEntity: Name: NameFull: Ehret Kasemo, Totta – PersonEntity: Name: NameFull: Oppmann, Maximilian – PersonEntity: Name: NameFull: Dembski, Sofia – PersonEntity: Name: NameFull: Steinke, Maria – PersonEntity: Name: NameFull: Lajtha, Elena – PersonEntity: Name: NameFull: Moratin, Helena – PersonEntity: Name: NameFull: Stöth, Manuel – PersonEntity: Name: NameFull: Scherzad, Agmal – PersonEntity: Name: NameFull: Delaval, Mathilde Noémie – PersonEntity: Name: NameFull: Zimmermann, Ralf – PersonEntity: Name: NameFull: Di Bucchianico, Sebastiano – PersonEntity: Name: NameFull: Hackenberg, Stephan – PersonEntity: Name: NameFull: Meyer, Till J. IsPartOfRelationships: – BibEntity: Dates: – D: 01 M: 10 Text: Oct2025 Type: published Y: 2025 Identifiers: – Type: issn-print Value: 13826689 Numbering: – Type: volume Value: 119 Titles: – TitleFull: Environmental Toxicology & Pharmacology Type: main |
| ResultId | 1 |