COVID, AMYLOID, AND INFLAMMATION
Literature collection of the CovAmInf workgroup.
Editors Joshua T. Berryman Abdul Mannan Baig Artemi Bendandi Daniel Bonhenry Mattheos A.G. Koffas
SARS-CoV-2 drives NLRP3 inflammasome activation in human microglia through spike protein (2022)
Eduardo A. Albornoz, Alberto A. Amarilla, Naphak Modhiran, Sandra Parker, Xaria X. Li, Danushka K. Wijesundara, Julio Aguado, Adriana Pliego Zamora, Christopher L. D. McMillan, Benjamin Liang, Nias Y. G. Peng, Julian D. J. Sng, Fatema Tuj Saima, Jenny N. Fung, John D. Lee, Devina Paramitha, Rhys Parry, Michael S. Avumegah, Ariel Isaacs, Martin W. Lo, Zaray Miranda-Chacon, Daniella Bradshaw, Constanza Salinas-Rebolledo, Niwanthi W. Rajapakse, Ernst J. Wolvetang, Trent P. Munro, Alejandro Rojas-Fernandez, Paul R. Young, Katryn J. Stacey, Alexander A. Khromykh, Keith J. Chappell, Daniel Watterson, Trent M. Woodruff
DOI: 10.1038/s41380-022-01831-0 PubMed: 36316366
The NLRP3 inflammasome activation leads to the release of pro-inflammatory cytokines and pyroptotic cell death, and is linked to neurodegenerative diseases. Protein aggregates such as alpha-synuclein, amyloid beta, TAR DNA-binding protein-43 and superoxidase-1 act as inducers.
The SARS-CoV-2 virus and spike protein by itself can activate the NLRP3 inflammasome in microglia cells.
