tetano
Editor, Senior Moderator
Respir Res
. 2022 Feb 10;23(1):25.
doi: 10.1186/s12931-022-01944-8.
Pulmonary vascular inflammation with fatal coronavirus disease 2019 (COVID-19): possible role for the NLRP3 inflammasome
Oindrila Paul[SUP] 1 [/SUP], Jian Qin Tao[SUP] 1 [/SUP], Eric West[SUP] 1 [/SUP], Leslie Litzky[SUP] 2 [/SUP], Michael Feldman[SUP] 2 [/SUP], Kathleen Montone[SUP] 2 [/SUP], Chamith Rajapakse[SUP] 3 [/SUP], Christian Bermudez[SUP] 4 [/SUP], Shampa Chatterjee[SUP] 5 [/SUP]
Affiliations
Abstract
Background: Pulmonary 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.
Methods: Lung 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.
Results: In 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.
Conclusion: Vascular 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.
Keywords: COVID-19; Lung inflammation; Mechanical ventilation; Microthrombosis; NLRP3 inflammasome; Vascular endothelium.
. 2022 Feb 10;23(1):25.
doi: 10.1186/s12931-022-01944-8.
Pulmonary vascular inflammation with fatal coronavirus disease 2019 (COVID-19): possible role for the NLRP3 inflammasome
Oindrila Paul[SUP] 1 [/SUP], Jian Qin Tao[SUP] 1 [/SUP], Eric West[SUP] 1 [/SUP], Leslie Litzky[SUP] 2 [/SUP], Michael Feldman[SUP] 2 [/SUP], Kathleen Montone[SUP] 2 [/SUP], Chamith Rajapakse[SUP] 3 [/SUP], Christian Bermudez[SUP] 4 [/SUP], Shampa Chatterjee[SUP] 5 [/SUP]
Affiliations
- PMID: 35144622
- DOI: 10.1186/s12931-022-01944-8
Abstract
Background: Pulmonary 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.
Methods: Lung 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.
Results: In 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.
Conclusion: Vascular 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.
Keywords: COVID-19; Lung inflammation; Mechanical ventilation; Microthrombosis; NLRP3 inflammasome; Vascular endothelium.