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COVID-19 May destroy lungs by promoting excessive release of sticky DNA web

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White blood cells, called neutrophils, are involved in severe cases of COVID-19. Neutrophils form sticky, microbially adherent neutrophil extracellular traps (NETs) in DNA, which can become overheated and damage the body’s own tissues. Neutrophils have already been involved in severe COVID-19 by studies linking SARS-CoV-2 associated lung pathology with numerous circulating neutrophils. Additional support-a large number of NETs distributed throughout the lungs and increased NETs in plasma-comes from two studies that appeared on September 14. Experimental Medical Journal (JEM).

First study,Neutrophil extracellular traps infiltrate the pulmonary airways, stroma, and vascular compartments of severe COVID-19The lungs of a patient from the University of Liège, led by Thomas Marishall, Cecil Urie, and Philippe Delben, who died of COVID-19 and showed histopathological features of diffuse alveolar injury. I found a considerable amount of NETs in different partitions of. In contrast, NETS said it was “not present in the lungs of patients who died from another cause.”

According to researchers, the NET often appeared to almost completely block the small bronchioles and alveoli that mediate gas exchange. NETs were also formed at the site of inflammation in the interstitial compartment between the alveoli and blood vessels, and were also found in the blood vessels themselves near small thrombi called microthrombus.

“NET was found in the inflammatory region rich in airway compartments and interstitial neutrophils, but NET-prone neutrophils were present in arteriole microthrombus,” wrote Malichal and colleagues. .. JEM.. “Our results support the hypothesis that NET may represent a driver of severe pulmonary complications of COVID-19, and the NET targeting approach is uncontrolled tissue damage and thrombotic response in COVID-19. It suggests that it can be considered for the treatment of. “

“NET can form a platform for the adhesion of platelets to other blood coagulation factors,” he explained. However, he added that further investigation is needed to determine whether NET actually contributes to the formation of COVID-19-related pulmonary microthrombus.

In the second study, “SARS-CoV-2 – Triggered Neutrophil Extracellular Traps Mediate COVID-19 PathologyA team of researchers led by Fernando Queiroz Cunha, Flavio Protasio Veras, and Thiago Mattar Cunha of the University of Sao Paulo also identified an increase in the number of NETs in the lungs of patients with severe COVID-19, and that NET formation was elevated in COVID. We also found the plasma of 19 patients.

“We have found that viable SARS-CoV-2 can directly induce the release of NET by healthy neutrophils,” the researchers emphasized. “Mechanically, the NET caused by SARS-CoV-2 depends on angiotensin converting enzyme 2, serine proteases, viral replication, and PAD-4.”

Finally, NET released from SARS-CoV-2 infected neutrophils was found to induce the death of laboratory-proliferated lung cells. However, researchers have found that inhibition of NET release or the degradation of NET by enzymes that chew DNA can prevent cell death.

“Our study” states that it supports the use of inhibitors of NET synthesis or promoters of NET fragmentation as a strategy to improve organ damage associated with severe COVID-19.

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