4.7 Article

Lung Inflammasome Activation in SARS-CoV-2 Post-Mortem Biopsies

Journal

Publisher

MDPI
DOI: 10.3390/ijms232113033

Keywords

COVID-19; inflammasome; pyroptosis; cytokine; immunohistochemistry; pulmonary tissue; oxidative stress

Funding

  1. CNPq [304356/2018-2]

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The activation of the inflammasome complex is significantly increased in COVID-19 patients, indicating its involvement in the pathogenesis of the disease. Additionally, levels of cell pyroptosis and inflammasome-derived cytokines are greatly elevated.
The inflammasome complex is a key part of chronic diseases and acute infections, being responsible for cytokine release and cell death mechanism regulation. The SARS-CoV-2 infection is characterized by a dysregulated cytokine release. In this context, the inflammasome complex analysis within SARS-CoV-2 infection may prove beneficial to understand the disease's mechanisms. Post-mortem minimally invasive autopsies were performed in patients who died from COVID-19 (n = 24), and lung samples were compared to a patient control group (n = 11) and an Influenza A virus H1N1 subtype group from the 2009 pandemics (n = 10). Histological analysis was performed using hematoxylin-eosin staining. Immunohistochemical (IHC) staining was performed using monoclonal antibodies against targets: ACE2, TLR4, NF-kappa B, NLRP-3 (or NALP), IL-1 beta, IL-18, ASC, CASP1, CASP9, GSDMD, NOX4, TNF-alpha. Data obtained from digital analysis underwent appropriate statistical tests. IHC analysis showed biomarkers that indicate inflammasome activation (ACE2; NF-kappa B; NOX4; ASC) were significantly increased in the COVID-19 group (p < 0.05 for all) and biomarkers that indicate cell pyroptosis and inflammasome derived cytokines such as IL-18 (p < 0.005) and CASP1 were greatly increased (p < 0.0001) even when compared to the H1N1 group. We propose that the SARS-CoV-2 pathogenesis is connected to the inflammasome complex activation. Further studies are still warranted to elucidate the pathophysiology of the disease.

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