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Activity of Tracheal Cytotoxin of Bordetella pertussis in a Human Tracheobronchial 3D Tissue Model
Zitieren Sie bitte immer diese URN: urn:nbn:de:bvb:20-opus-222736
- Bordetella pertussis is a highly contagious pathogen which causes whooping cough in humans. A major pathophysiology of infection is the extrusion of ciliated cells and subsequent disruption of the respiratory mucosa. Tracheal cytotoxin (TCT) is the only virulence factor produced by B. pertussis that has been able to recapitulate this pathology in animal models. This pathophysiology is well characterized in a hamster tracheal model, but human data are lacking due to scarcity of donor material. We assessed the impact of TCT and lipopolysaccharideBordetella pertussis is a highly contagious pathogen which causes whooping cough in humans. A major pathophysiology of infection is the extrusion of ciliated cells and subsequent disruption of the respiratory mucosa. Tracheal cytotoxin (TCT) is the only virulence factor produced by B. pertussis that has been able to recapitulate this pathology in animal models. This pathophysiology is well characterized in a hamster tracheal model, but human data are lacking due to scarcity of donor material. We assessed the impact of TCT and lipopolysaccharide (LPS) on the functional integrity of the human airway mucosa by using in vitro airway mucosa models developed by co-culturing human tracheobronchial epithelial cells and human tracheobronchial fibroblasts on porcine small intestinal submucosa scaffold under airlift conditions. TCT and LPS either alone and in combination induced blebbing and necrosis of the ciliated epithelia. TCT and LPS induced loss of ciliated epithelial cells and hyper-mucus production which interfered with mucociliary clearance. In addition, the toxins had a disruptive effect on the tight junction organization, significantly reduced transepithelial electrical resistance and increased FITC-Dextran permeability after toxin incubation. In summary, the results indicate that TCT collaborates with LPS to induce the disruption of the human airway mucosa as reported for the hamster tracheal model.…
Autor(en): | David K. Kessie, Nina Lodes, Heike Oberwinkler, William E. Goldman, Thorsten Walles, Maria Steinke, Roy Gross |
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URN: | urn:nbn:de:bvb:20-opus-222736 |
Dokumentart: | Artikel / Aufsatz in einer Zeitschrift |
Institute der Universität: | Fakultät für Biologie / Theodor-Boveri-Institut für Biowissenschaften |
Medizinische Fakultät / Lehrstuhl für Tissue Engineering und Regenerative Medizin | |
Sprache der Veröffentlichung: | Englisch |
Titel des übergeordneten Werkes / der Zeitschrift (Englisch): | Frontiers in Cellular and Infection Microbiology |
ISSN: | 2235-2988 |
Erscheinungsjahr: | 2021 |
Band / Jahrgang: | 10 |
Aufsatznummer: | 614994 |
Originalveröffentlichung / Quelle: | Frontiers in Cellular and Infection Microbiology 2021, 10:614994. doi: 10.3389/fcimb.2020.614994 |
DOI: | https://doi.org/10.3389/fcimb.2020.614994 |
Allgemeine fachliche Zuordnung (DDC-Klassifikation): | 6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit |
Freie Schlagwort(e): | Bordetella pertussis; airway epithelia; ciliostasis; tight junction; tissue model; tracheal cytotoxin |
Datum der Freischaltung: | 16.03.2021 |
Datum der Erstveröffentlichung: | 19.01.2021 |
Open-Access-Publikationsfonds / Förderzeitraum 2020 | |
Lizenz (Deutsch): | CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International |