Journal
JOURNAL OF LEUKOCYTE BIOLOGY
Volume 78, Issue 2, Pages 325-337Publisher
WILEY
DOI: 10.1189/jlb.0105017
Keywords
mice; human; death-receptor pathway; mitochondrial pathway; immune and organ dysfunction
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Funding
- NHLBI NIH HHS [HL 73525] Funding Source: Medline
- NIGMS NIH HHS [GM 53209] Funding Source: Medline
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Sepsis and multiple organ failure continue to be significant problems among trauma, burn, and the critically ill patient population. Thus, a number of laboratories have focused on understanding the role of altered apoptotic cell death in contributing to immune and organ dysfunction seen in sepsis and shock. Immune cells that undergo altered apoptotic changes include neutrophils, macrophages, dendritic cells, as well as various lymphocyte populations. Evidence of epithelial as well as endothelial cell apoptotic changes has also been reported. Although mediators such as steroids, tumor necrosis factor, nitric oxide, C5a, and Fas ligand (FasL) appear to contribute to the apoptotic changes, their effects are tissue-and cell population-selective. As inhibiting Fas-FasL signaling (e.g., gene deficiency, Fas fusion protein, or Fas short interfering RNA administration), caspase inhibition (caspase mimetic peptides), and/or the overexpression of downstream antiapoptotic molecules (e.g., Bcl-2, Akt) improve survival of septic mice, it not only demonstrates the pathological significance of this process but points to novel targets for the treatment of sepsis.
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