According to two new studies published on September 14 in the Journal of Experimental Medicine (JEM), sticky DNA WEB released through immune cells known as neutrophils can cause much tissue damage related to severe COVID-19 infections. in Belgium and Brazil, he suggests that blocking the release of these DNA networks may simply be a new healing target for controlling the serious COVID-19 bureaucracy.
While many other people inflamed with SARS-CoV-2 have mild symptoms, some patients develop an exaggerated inflammatory reaction that can damage the lungs and cause acute respiratory distress syndrome (EDS), resulting in low oxygen levels in the blood. and, potentially, the patient Death. An early indicator of severe COVID-19 is an increased number of circulating neutrophils, a type of white blood motive. Neutrophils can trap and kill invading microbes by unwinding their DNA and extruding it from the motive to form sticky networks called extramobile neutrophil traps ( NETs) However, neural tube defects can also damage surrounding tissues and thus can cause some of the severe COVID-19-related lung diseases.
In one of the new studies, a study team from the GIGA Institute at the University of Liege, led by Thomas Marichal, Cécile Oury and Philippe Delvenne, examined the lungs of patients who had succumbed to COVID-19 and discovered a large number of ENTs. Researchers saw many NNSs in the airway compartment, where they seemed to almost completely clog the small bronchioles and alveoli that mediate fuel exchanges. , and can even be seen in blood vessels near small blood clots called micro-thrombus that can limit blood flow to the lungs and are an unusual pathological feature of severe patients with COVID-19.
NNEs would possibly shape a plaque for platelet adhesion and other blood clotting factors, but if NTDs contribute to the formation of COVID-19-related pulmonary microtrombos it will require further research. 19 patients can help clinically control severe forms of COVID-19 by mitigating thrombotic events, as well as inflammation that damages tissue damage, fibrosis and airway obstruction. “
At the time of the study, a team of researchers led by Fernando Queiroz Cunha, Flavio Protasio Veras and Thiago Mattar Cunha of the University of Sao Paulo also experienced an increase in the amount of ETD in the lungs of severe PATIENTS with COVID-19 and found that the formation of TNE was also superior in blood plasma in patients with COVID-19. In addition, the researchers decided that SARS-CoV-2 can cause NTD to release by infecting neutrophils and replicating them internally. inflammations with SARS-CoV-2 induce death in laboratory-grown lung mobiles, the researchers discovered, but mobile death is prevented if net release is inhibited or neural tube defects degrade through an enzyme that chews DNA.
“Our study supports the use of NET synthesis inhibitors or promoters of TNE fragmentation as a strategy for coVID-19 severe organic damage,” explains Fernando Queiroz Cunha.
Rockefeller University Press
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