Determine how SARS-CoV-2, a virus that causes COVID-19, moves from the initial stage of infection, when patients are usually asymptomatic, to a later stage in which people may experience life-threatening inflammation in in the lungs, is an important step. to understand how to attack and treat the disease effectively. But this process of change is complex and cannot be studied as easily as it occurs in the human body.
Using a laboratory model similar to the previous model to study cystic fibrosis, lung cancer, Emory University researchers were able to replicate this complex interaction. By doing so, they identified the key pathogen that causes the change from the beginning to the end of COVID-19 and were able to test a candidate’s antibodies against those. Cellsthey show their effect on the elimination of bacteria and inflammation.
The results of this new search are now in print and online as an access point Cell Report. The study concluded that it entered the lungs monocytes (a type of immune cell that can migrate into tissues) induces the development of inflammatory mediators in COVID-19 and is an important target for treatment. In addition, the study provided detailed information on how antibiotics are administered remdesivir and the immunomodulator baricitinib can be used alone or in combination to attack these monocytes.
“SARS-CoV-2 is really voting in the way immune system job. Serious factors indicate inactivity immune responseand unfortunately, we do not understand why some patients are more susceptible to this negative response, and others are less prone to it, “said lead author Rabindra Tirouvanziam, Ph.D., an immunologist and professor at Department of Pediatrics at Emory University School of Medicine. improve patient outcomes. “
Significance, documentation and lab data obtained in a laboratory model mirror in vivo data collected from hospital COVID-19 patients. Since systemic change is very difficult to observe in patients, this study provides a missing data link and a way to better understand how and when COVID-19 treatment may work best.
The model used in the study simulates a series of events that occur when a person is exposed to COVID-19. It is based on the growth of human epithelial cells that line the lungs with the top of their lungs exposing them to air. These cells are infected with SARS-CoV-2 and the product allows blood monocytes to migrate to the infected epithelium, where they become infected. Anti-COVID-19 drugs can be added at any location to measure how they affect infection and the immune response in epithelial cells and monocytes entering the lungs at different stages.
In the early stages of SARS-CoV-2 infection, the virus replicates rapidly but avoids attracting the “first-response” immune cells – called neutrophils – that can begin to swell early and eliminate the virus. An infected person does not cause symptoms, and in fact, may recur and then clear the virus without any symptoms. But in the end, monocytes also respond; these antibiotics live longer neutrophils and it can spread to the lungs to get the virus and copy its genetic material, which tells the body to increase its immune response. It is a highly addictive substance that can cause excessive swelling.
“Disruption is the problem,” Tirouvanziam said. “No living organism remains but the monocytes entering the lungs will find and replicate its mechanism and continue the immune response, so the inflammation is permanent and can multiply rapidly.”
The study found that the combination of the two treatments approved by the FDA for COVID-19-remdesivir and baricitinib — enhances the immune response and protection against monocytes infected with SARS-CoV-2. It sheds light on the therapeutic timing as a key to eliminating acute inflammation, which can lead to life-threatening conditions known as acute respiratory distress syndrome.
The small sample size in this study differs in that it uses human body cells in a system that mimics lung conditions. Tirouvanziam says this is an improved platform to test additional drugs on the SARS-CoV-2 variant. “It is important to note that this is not the end. There are new differences that arise on a regular basis, and in the future we may be exposed to these possibilities several times a year. Addressing these differences,” he said. Tirouvanziam.
Brian Dobosh et al, Baricitinib enhances the proinflammatory phase of COVID-19 by which monocytes enter the lungs, Cell Report (2022). DOI: 10.1016 / j.celrep.2022.110945
hintImmunologists have discovered a key immunological target for treating COVID-19 ions (2022, June 14) Retrieved 14 June 2022 from https://medicalxpress.com/news/2022-06-immunologists-critical-immune- cell-covid-.html
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