Modelling SARS-CoV-2 infection in a human alveolus microphysiological system

2024 · doi:10.1099/acmi.0.000814.v2
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The paper describes an adaptation of a human alveolus microphysiological system (MPS) using primary alveolar epithelial and lung microvascular endothelial cells to model SARS-CoV-2 infection under BSL3 conditions. Using the air-liquid interface with breathing-like stretch, the authors report clinically relevant cytopathic effects, including rounding of alveolar type 2 cells and disruption of the tight junction protein occludin, with viral replication supported by nucleocapsid immunocytochemistry and increased virus shedding within two days. They also observe associated changes in innate host immune responses. The study’s main limitation is that it models SARS-CoV-2 infection in lung alveolar cells rather than demonstrating generalizable mechanisms across other tissues or conditions. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

The COVID-19 pandemic has highlighted the importance of physiologically relevant in vitro models to assist preclinical research. Here, we describe the adaptation of a human alveolus microphysiological system (MPS) model consisting of primary human alveolar epithelial and lung microvascular endothelial cells to study infection with SARS-CoV-2 at Biosafety Level 3 (BSL3) facility. This infection model recapitulates breathing-like stretch and culture of epithelial cells at the air-liquid interface (ALI) and resulted in clinically relevant cytopathic effects including cell rounding of alveolar type 2 cells (AT2) and disruption of the tight junction protein occludin (OCLN). Viral replication was confirmed by immunocytochemical nucleocapsid staining in the epithelium and increased shedding of SARS-CoV-2 virus within two days post-infection, associated with changes in innate host immune responses. Together, these data demonstrate that, under the experimental conditions used in this work, this human alveolus MPS chip can successfully model SARS-CoV-2 infection of human alveolar lung cells.
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Full text loading... Abstract The COVID-19 pandemic has highlighted the importance of physiologically relevant in vitro models to assist preclinical research. Here, we describe the adaptation of a human alveolus microphysiological system (MPS) model consisting of primary human alveolar epithelial and lung microvascular endothelial cells to study infection with SARS-CoV-2 at Biosafety Level 3 (BSL3) facility. This infection model recapitulates breathing-like stretch and culture of epithelial cells at the air-liquid interface (ALI) and resulted in clinically relevant cytopathic effects including cell rounding of alveolar type 2 cells (AT2) and disruption of the tight junction protein occludin (OCLN). Viral replication was confirmed by immunocytochemical nucleocapsid staining in the epithelium and increased shedding of SARS-CoV-2 virus within two days post-infection, associated with changes in innate host immune responses. Together, these data demonstrate that, under the experimental conditions used in this work, this human alveolus MPS chip can successfully model SARS-CoV-2 infection of human alveolar lung cells. - Received: - Version Posted: Funding - U.S. Food and Drug Administration (Award 75F40120C00085) - Principal Award Recipient: Simon GP Funnell - Biotechnology and Biological Sciences Research Council (Award BB/CCG2260/1) - Principal Award Recipient: George M. Savva

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