Since the outbreak of the Covid-19 pandemic, Sars-Cov-2 coronavirus infection has been associated to severe interstitial pneumonia and forms of acute respiratory failure with clinical features distinct from those caused by bacterial infections or other viruses. Some research has suggested that the immune response triggered by Sars-Cov-2 differs from that to other respiratory infections without clarifying exactly the reasons for the different etiology. In this sense, researchers from the Feinberg School of Medicine at Northwestern University in Evanston, Illinois, have provided a first comparison of immune mechanisms contributing to Covid-19 pneumonia and those involved in pneumonia caused by other infections, highlighting important differences from other types of pneumonia.
To advance the analysis, the researchers examined immune cells obtained from bronchoalveolar lavage samples from patients with Covid-19 and compared them with those collected from patients with pneumonia caused by other pathogens, identifying how these immune cells drive inflammation. A level of resolution “which could never be achieved without directly sampling lung fluid – explained Dr. Alexander Misharin, senior co-author of the study -. Patient samples were analyzed with the most sophisticated technologies available in Northwestern research labs, requiring the concerted effort of over 100 researchers”.
The results of the study, published in the journal Nature, indicate that, instead of rapidly infecting large regions of the lung, the coronavirus Sars-Cov-2 settles in small areas, by hijacking the immune cells of the lungs and using them to spread through these organs for days or even weeks, like multiple fires spreading across a forest. This causes the infection to slowly move through lung tissues, leaving damage behind and continuously fueling fever, low blood pressure, and damage to the kidneys, brain, heart, and other organs in Covid-19 patients. “The serious complications of the infection da coronavirus Sars-Cov-2 – the authors say – they could be related to the long course of the disease rather than a more serious disease”.
Researchers have thus identified the critical targets for treating Covid-19 pneumonia and reducing its damage, in particular macrophages – immune cells typically charged with protecting the lungs – which can become infected with Sars-Cov-2 and contribute to the spread of the infection through the lung, thus paving the way for the testing of new drugs. The clinical trial is expected in early 2021, with the goal of calm the inflammatory response of these immune cells and allow the repair process of damaged lung tissues to start. “Our wish – the researchers conclude – is to try to make Covid-19 a mild disease rather than a serious one, therefore comparable to a bad cold”.
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