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Pyroptotic cell corpses are crowned with F-actin-rich filopodia that engage CLEC9A signaling in incoming dendritic cells.
Nat Immunol
December 2024
Institute for Molecular Bioscience, University of Queensland, Brisbane, Queensland, Australia.
While apoptosis dismantles the cell to enforce immunological silence, pyroptotic cell death provokes inflammation. Little is known of the structural architecture of cells undergoing pyroptosis, and whether pyroptotic corpses are immunogenic. Here we report that inflammasomes trigger the Gasdermin-D- and calcium-dependent eruption of filopodia from the plasma membrane minutes before pyroptotic cell rupture, to crown the resultant corpse with filopodia.
View Article and Find Full Text PDFPostmortem interval estimation of time since death: impact of non-histone binding proteins, immunohistochemical, and histopathological changes in vivo.
J Med Life
September 2024
Anatomy Department, Faculty of Medicine, Al-Baha University, Al-Baha, KSA.
The postmortem interval (PMI) is one of the primary objectives and challenging tasks proposed for determining the time of death. This study aimed to estimate the PMI using serum levels of high mobility group box 1 (HMGB1), a biomarker of pyroptotic cell death, along with desmin immunohistochemical and histological analyses of the gastrocnemius muscle in rats at various time intervals. Serum and gastrocnemius muscle samples were collected at zero, 24-, 48-, 72-, and 96 hours postmortem from 50 rats maintained at 22 ± 2°C.
View Article and Find Full Text PDFCell organelles are retained inside pyroptotic corpses during inflammatory cell death.
Biosci Rep
October 2023
Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, U.S.A.
Many proinflammatory proteins are released via the necrotic form of cell death known as pyroptosis. Sometimes known as gasdermin D (GSDMD) dependent cell death, pyroptosis results from the formation of pores in the plasma membrane leading to eventual cell lysis. Seeking to understand the magnitude of this cell lysis we measured the size of proteins released during pyroptosis.
View Article and Find Full Text PDFIL-1β, IL-18, and eicosanoids promote neutrophil recruitment to pore-induced intracellular traps following pyroptosis.
Eur J Immunol
December 2016
Department of Microbiology and Immunology, Center for Gastrointestinal Biology and Disease, and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Inflammasomes activate caspase-1, initiating a lytic form of programmed cell death termed pyroptosis, which is an important innate immune defense mechanism against intracellular infections. We recently demonstrated in a mouse infection model of pyroptosis that instead of releasing bacteria into the extracellular space, bacteria remain trapped within the pyroptotic cell corpse, termed the pore-induced intracellular trap (PIT). This trapping mediates efferocytosis of the PIT and associated bacteria by neutrophils; bacteria are subsequently killed via neutrophil ROS.
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