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Modulating the Barrier Function of Human Alveolar Epithelial (hAELVi) Cell Monolayers as a Model of Inflammation.
Metz, Julia Katharina Wiegand, Birgit Schnur, Sabrina Knoth, Katharina Schneider-Daum, Nicole Groß, Henrik Croston, Glenn Reinheimer, Torsten Michael Lehr, Claus-Michael Hittinger, Marius
Metz, Julia Katharina
Wiegand, Birgit
Schnur, Sabrina
Knoth, Katharina
Schneider-Daum, Nicole
Groß, Henrik
Croston, Glenn
Reinheimer, Torsten Michael
Lehr, Claus-Michael
Hittinger, Marius
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2021-01-29
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The incidence of inflammatory lung diseases such as acute respiratory distress syndrome (ARDS) remains an important problem, particularly in the present time with the Covid-19 pandemic. However, an adequate in vitro test system to monitor the barrier function of the alveolar epithelium during inflammation and for assessing anti-inflammatory drugs is urgently needed. Therefore, we treated human Alveolar Epithelial Lentivirus-immortalised cells (hAELVi cells) with the pro-inflammatory cytokines TNF-α (25 ng/ml) and IFN-γ (30 ng/ml), in the presence or absence of hydrocortisone (HC). While TNF-α and IFN-γ are known to reduce epithelial barrier properties, HC could be expected to protect the barrier function and result in an anti-inflammatory effect. We investigated the impact of anti-inflammatory/inflammatory treatment on transepithelial electrical resistance (TEER) and the apparent permeability coefficient (P app ) of the low permeability marker sodium fluorescein (NaFlu). After incubating hAELVi cells for 48 hours with a combination of TNF-α and IFN-γ, there was a significant decrease in TEER and a significant increase in the P app . The presence of HC maintained the TEER values and barrier properties, so that no significant P app change was observed. By using hAELVi cells to study anti-inflammatory drugs in vitro, the need for animal experiments could be reduced and pulmonary drug development accelerated.
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Altern Lab Anim. 2021 Jan 29:261192920983015. doi: 10.1177/0261192920983015. Epub ahead of print.
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en
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0261-1929
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Attribution-NonCommercial-ShareAlike 4.0 International