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Cell death during sepsis: integration of disintegration in the inflammatory response to overwhelming infection

Authors
  • Pinheiro da Silva, Fabiano1
  • Nizet, Victor2
  • 1 University of California San Diego, Department of Pediatrics, School of Medicine, 9500 Gilman Drive, La Jolla, CA, 92093-0687, USA , La Jolla (United States)
  • 2 University of California San Diego, Skaggs School of Pharmacy & Pharmaceutical Sciences, 9500 Gilman Drive, La Jolla, CA, 92093-0687, USA , La Jolla (United States)
Type
Published Article
Journal
APOPTOSIS
Publisher
Springer-Verlag
Publication Date
Feb 07, 2009
Volume
14
Issue
4
Pages
509–521
Identifiers
DOI: 10.1007/s10495-009-0320-3
Source
Springer Nature
Keywords
License
Green

Abstract

Sepsis is a major health problem and a leading cause of death worldwide. In recent years, a crescendo of attention has been directed to the mechanisms of cell death that develop during this disease, since these are viewed as important contributors to the proinflammatory and anti-inflammatory responses associated with poor outcome. Here we discuss mechanisms of cell death evident severe bacterial infection and sepsis including necrosis, apoptosis, pyroptosis, and extracellular trap-associated neutrophil death, with a particular emphasis on lymphocyte apoptosis and its contribution to the immunosuppressed phenotype of late sepsis. Individual bacterial pathogens express virulence factors that modulate cell death pathways and influence the sepsis phenotype. A greater knowledge of cell death pathways in sepsis informs the potential for future therapies designed to ameliorate immune dysfunction in this syndrome.

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