New research has found that a combination treatment strategy targeting SARS-CoV-2 symptoms and severe lung injury is key to minimizing pulmonary sequelae – the chronic complications resulting from COVID-19 infection. The study was published in the “Clinical Microbiology Reviews Journal”.
Therapy using lung epithelial stem and progenitor cells has shown promise in mitigating the potentially deadly and highly damaging virus-induced inflammatory storm that can occur in severe cases of COVID-19, said Huaiyong Chen, PhD, principal investigator. at Tianjin Institute of Respiratory Diseases, and Director of Tianjin Key Laboratory of Lung Regenerative Medicine, Haihe Hospital, Tianjin University, China. “To minimize lung damage, we must effectively promote tissue regeneration by activating surviving lung stem and progenitor cells, or by directly transplanting healthy lung stem and progenitor cells into damaged lungs,” Chen said.
Both cell types can differentiate into pulmonary epithelial cells, which line the inner surfaces of the lungs where air exchange occurs. By doing so, they can repair lung damage caused by SARS-CoV-2, including fibrosis. The first step towards activating these regenerative cells is to prime the tissue environment with mesenchymal stem cells. These cells do not normally reside in the lungs, but when transplanted there, they secrete growth factors that promote the growth and differentiation of lung epithelial stem and progenitor cells. This, in turn, can repair the damage. Researchers are currently using animal models to determine the best way to achieve this.
But in severe cases, these regenerative cells can be damaged by cytokines, which are produced by immune cells in excess numbers during lung inflammation, preventing full restoration of lung structure and function. In such cases, healthy stem and progenitor cells may need to be transplanted into a person’s lungs. However, as with any transplant, immune rejection is likely to be a problem. It may be possible to use gene-editing technology, known as CRISPR, to modify these cells to reduce immunogenicity before transplantation, a possibility Chen is investigating.
For less severe cases, researchers will need to look for compounds that enhance the ability of progenitor and stem cells to trigger lung repair and regeneration following these injuries. Previous research had shown that certain compounds that target signaling pathways in stem and progenitor cells showed potential to improve lung regeneration in patients with asthma and pulmonary fibrosis. They can do the same for patients with SARS-CoV-2.
The impetus for the current study was Chen’s discovery that even 12 years after recovery, some survivors of the closely related virus, severe acute respiratory syndrome (SARS), first identified in 2003, were living with multiple sequelae. , reducing the quality of life. “I realized then that something had to be done to maximize lung regeneration, repair and recovery,” Chen said. (ANI)
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