| Autor: |
Cayford, Justin, Eccleston, Mark, Berman, Benjamin, Serneo, Finley, Kelly, Terry, Retter, Andrew, Zukas, Kieran |
| Zdroj: |
Blood; November 2023, Vol. 142 Issue: 1, Number 1 Supplement 1 p2542-2542, 1p |
| Abstrakt: |
Sepsis is a leading cause of death, affecting 1.7 million adults annually in the US, where it is implicated in ~350,000 deaths (1). Rapid recognition and intervention are required to avoid progression to septic shock and death. Sepsis results from a dysregulated host response to infection (2). We aimed to study part of this dysregulated response by analyzing NETosis in neutrophils. Neutrophils are integral to the innate immune response. They can undergo a unique type of programmed cell death, NETosis, where nuclear chromatin is extruded out of the cell to capture and deactivate pathogens and prevent dissemination. These neutrophil extracellular traps (NETs) contain nucleosomes, DNA and histone proteins. NETs help to trap invading pathogens but in excess, lead to endothelial damage, excessive activation of platelets and promote microthrombosis in distal organs leading to organ failure. Our understanding of NETosis largely stems from mouse models, immortalized cell lines, and isolated neutrophils. However, these don't entirely mirror the complexity of human immune response. Here we present a model of ex vivoNETosis induction in whole blood, which can be used to provide greater clarity on the complex signaling and chromatin changes associated with NETosis. |
| Databáze: |
Supplemental Index |
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