A group of researchers has grown a lung-model in the lab that mimics the alveoli, which are fragile lung air sacs where lung damage as well as the COVID-19 infection occurs. This advancement has allowed Duke University researchers to observe the fight between lung cells and the SARS-CoV-2 cells at great molecular scale.
The SARS-CoV-2 virus harms the alveoli. This leads to acute respiratory distress and pneumonia, which is the main cause of death in coronavirus patients. Researchers have been hindered in coronavirus studies due to the absence of experimental models that imitate human lung tissues.
However, the team, led by Purushothama Rao Tata who is a cell biologist at Duke, has created a model using mini-lungs. To grow the organoids, AT2 cells are used. These are the stem cells that mend the parts of the lungs where SARS-CoV-2 strikes.
Prior research at Duke had demonstrated that single alveolar epithelial type-2 cells, when isolated in small dishes, multiply into millions of cells that amass into organoids that look like alveoli. These lung organoids will allow high output science, in which many experiments can be undertaken concurrently to identify the chemical lung cells produce to respond to an infection or to screen for new drug candidates.
Tata explained that the model system allowed researchers to study respiratory viruses, such as influenza, that target lung cells, in addition to studying SARS-CoV-2. “Stem Cell” journal featured the paper, which described the growth-process of the mini-lungs as well as some experiments with the COVID-19 infection, online on October 21.
The researchers worked together with their virology colleagues from the University of North Carolina and Duke to study the SARS-CoV-2 infection using the mini-lungs. Additionally, they used the advanced biosafety level 3 amenities at UNC-CH and Duke to safely handle and expose the lung organoids to the deadly viral infection. They then observed the chemical signals and the gene activity the lung cells produced after infection.
The paper’s co-author, Ralph Baric, said that this was a major breakthrough as they used cells that did not have purified cultures. Baric, a distinguished professor of microbiology, immunology and epidemiology at UNC, heads that lab that was used to confirm that COVID-19 targeted the ACE2 cell surface receptor, which led to an infection.
The lung organoids launched an inflammatory response that was brought about by interferons when the lungs were infected with the deadly virus. The scientists also noted that the lungs launched a cytokine storm of immune molecules to counter the virus.
Baric stated that his lab would use the lung organoids to better understand the dominant version of the SARS-CoV-2 virus, a new strain referred to as D614G. This strain is even more infectious as it is more efficient at recognizing lung cell ACE2 receptors.
On the other hand, Tata explained that his group would be collaborating with industry and academic partners to utilize the organoids for cell-based therapies and, in the future, work on growing a whole lung for transplantation.
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