Time for A Breather…Pulmonary Research During the COVID-19 Pandemic

March 16, 2021

By Andrea Picon

As we enter week 5 of Coronavirus confinement, the reality that the world has changed not only rings in my ears from multiple news outlets, but is also seen in plain sight across our communities. As we have done during past global crises, we must again do now…ADAPT!

During this COVID19 confinement period, Flexcell is one of the few, lucky companies classified as an essential business to supply research laboratories and facilities world-wide. I am inspired by our staff, who have continued to work hard to keep our business operations functioning. Customer Support has been taking orders, making RFQs and answering questions to our research community. Our Engineering and Production teams have been working with our suppliers to continue manufacturing needed equipment and consumables for our end users. Thanks to all our employees, suppliers and customers who have helped keep our business alive during the COVID19 crisis.

Speaking of adaptation, that is exactly what viruses do best! Viruses are described as neither living nor dead particles that have a parasitic-like relationship with the living cells it needs to thrive. Scientists are helping to explain what, where and how the novel 2019 Coronavirus has become one of the deadliest pandemics in the last century. There are many published articles on the origin of COVID19, I would like to highlight a recent paper, which debunks the argument that this virus has been purposely altered and released into the public domain. A March 2020 study published in Nature Medicine by researchers at the Scripps Research Institute and Tulane University School of Medicine used bioinformatic tools to analyze the publicly available genomic data on several coronaviruses, including that of COVID19. Researchers found their spike proteins contain unique adaptions of the novel 2019 coronavirus, which provides the possibility to bind to a specific protein on human cells called Angiotensin Converting Enzyme 2 (ACE2).The related coronavirus that causes severe Acute Respiratory Syndrome (or SARS-COVvirus) binds to the same ACE2. Ironically, ACE2 enzymes help protect us from the lung damage. Based on computer modeling, scientists’ early hypothesis was that COVID19 would not bind as easily to human cells, as the SARS-COV virus. Unfortunately, COVID19 binds far better than predicted, which could possibly be due to natural selection on ACE2 enzyme and another previously unknown alternate binding site.

As I write this blog, promising research is being done on antibodies that may give guidance on how to neutralize it. An April 2020 paper published in Science from researchers at Scripps Research Institute and University of Hong Kong analyzes the structural make-up of the novel 2019 coronavirus. They are looking at how the CR3022 antibody may be used to bind and attack COVID19. CR3022 binds to a similar location (receptor binding domain or RBD) on both the COVID19 and SARS-COV coronaviruses. That site differs by only 4 amino acids. The groups have found that the CR3022 antibody can only bind when at least 2 RBDs on the spike protein are in a certain position on the virus (both “up” and slightly rotated). Curiously, the CR3022 antibody does not come from patients, who have recovered from COVID19, but two decades earlier from patients of the SARS-COV outbreak. More data and samples are being collected,but the research being done by these global teams is helping get closer to potential vaccines against the virus.

We know the COVID19 attacks the respiratory system, specifically the lungs, as well as, other vital organs. Other studies performed in the field of Pulmonary research, where Flexcell® Tension Systems are being used to understand:

·       lung cell signaling inflammatory response and regulation

·       lung-specific gene expression and mRNA response to mechanical stretch

·       cytokine protein expression through cyclic stretch

·       ventilator-induced lung injury studies

·       alveolar macrophage biomarkers from stretch-induced apoptosis

·       lung tissue and alveolar epithelial cell repair studies

Lung Publications Using Flexcell® Tension Systems

There are over 30 new COVID19 grants and funding available through the NIH/NIAD/NIGMS/NHLBI and other government agencies. To learn more:

Flexcell® is looking for scientists interested in Pulmonary research areas utilizing our cell-stretching bioreactor technology. Please contact our team at to learn more about our products and how we may be able to help support your research needs!



Andersen, K.G., Rambaut,A., Lipkin, W.I. et al. The proximal origin of SARS-CoV-2. Nat Med 26, 450–452 (2020).

Meng Yuan, Nicholas C. Wu, XueyyongZhu, Chang-Chun D. Lee, Ray T.Y. So, Huibin Lv, Chris K. P. Mok, Ian A, Wilson. A highly conservative cryptic epitope in the receptor-binding domains of SARS-COV-2 and SARS-COV. Science: 03April2020. DOI: 10.1126/science.abb7269.

Nicholls John, Peris Malik. Good ACE,bad ACE do battle in lung injury, SARS. Nature Medicine Volume 11, number 8, August 2005:

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