Abstract
BackgroundPulmonary hyperinflammation is a key event with SARS-CoV-2 infection. Acute respiratory distress syndrome (ARDS) that often accompanies COVID-19 appears to have worse outcomes than ARDS from other causes. To date, numerous lung histological studies in cases of COVID-19 have shown extensive inflammation and injury, but the extent to which these are a COVID-19 specific, or are an ARDS and/or mechanical ventilation (MV) related phenomenon is not clear. Furthermore, while lung hyperinflammation with ARDS (COVID-19 or from other causes) has been well studied, there is scarce documentation of vascular inflammation in COVID-19 lungs.MethodsLung sections from 8 COVID-19 affected and 11 non-COVID-19 subjects, of which 8 were acute respiratory disease syndrome (ARDS) affected (non-COVID-19 ARDS) and 3 were from subjects with non-respiratory diseases (non-COVID-19 non-ARDS) were H&E stained to ascertain histopathological features. Inflammation along the vessel wall was also monitored by expression of NLRP3 and caspase 1.ResultsIn lungs from COVID-19 affected subjects, vascular changes in the form of microthrombi in small vessels, arterial thrombosis, and organization were extensive as compared to lungs from non-COVID-19 (i.e., non-COVID-19 ARDS and non-COVID-19 non-ARDS) affected subjects. The expression of NLRP3 pathway components was higher in lungs from COVID-19 ARDS subjects as compared to non-COVID-19 non-ARDS cases. No differences were observed between COVID-19 ARDS and non-COVID-19 ARDS lungs.ConclusionVascular changes as well as NLRP3 inflammasome pathway activation were not different between COVID-19 and non-COVID-19 ARDS suggesting that these responses are not a COVID-19 specific phenomenon and are possibly more related to respiratory distress and associated strategies (such as MV) for treatment.
Highlights
It has been more than two years since the pandemic caused by the novel SARS-CoV-2 corona virus, known as COVID-19 has affected large populations globally [1, 2]
All sections from lungs of COVID-19 acute respiratory distress syndrome (ARDS), non-COVID-19 ARDS subjects stained positively for the NOD-like receptor protein 3 (NLRP3) inflammasome associated markers that were assessed by fluorescence imaging
Taken together, our data show that NLRP3 inflammasome pathway activation was not different between COVID-19 and non-COVID-19 ARDS suggesting that this pathway is not COVID-19 specific and is possibly more related to respiratory distress
Summary
It has been more than two years since the pandemic caused by the novel SARS-CoV-2 corona virus (severe acute respiratory syndrome coronavirus), known as COVID-19 has affected large populations globally [1, 2]. COVID-19 may progress to acute respiratory distress syndrome (ARDS) [9, 10]; incidence of ARDS with COVID-19 is about 33%. Histological, biochemical and physiological studies of COVID-19 have shown extensive inflammation and injury, but the extent to which these are a COVID19 specific, or an ARDS related phenomenon is not clear. While lung hyperinflammation with ARDS (whether from COVID-19 or from other causes) has been well studied, there is scarce documentation of vascular inflammation in COVID-19 affected lungs [7, 14]. Numerous lung histological studies in cases of COVID-19 have shown extensive inflammation and injury, but the extent to which these are a COVID-19 specific, or are an ARDS and/or mechanical ventilation (MV) related phenomenon is not clear. While lung hyperinflammation with ARDS (COVID-19 or from other causes) has been well studied, there is scarce documentation of vascular inflammation in COVID-19 lungs
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