sFas and sFas Ligand and Pediatric Sepsis-Induced Multiple Organ Failure Syndrome

Doughty, Lesley; Clark, Robert S. B.; Kaplan, Sandra S.; Sasser, Howell; Carcillo, Joseph A.

doi:10.1203/00006450-200212000-00018

Cited by 52 publications

(41 citation statements)

References 42 publications

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“…The clinical relevance of infected neonatal neutrophils having an increase surface expression of Fas and Fas ligand and release of sFasL is supported by previous studies showing that the development of multiple organ failure, specifically hepatic failure was demonstrated in patients with viral infections with increased sFasL levels (35). These findings have also been noted in human and animal studies related to HSV infection (36,37).…”

Section: Discussionmentioning

confidence: 58%

Induction of Apoptosis by Herpes Simplex Virus-1 in Neonatal, But Not Adult, Neutrophils

et al. 2006

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ABSTRACT:We report a study on the effect of herpes simplex virus 1 (HSV-1) infection on apoptosis of neutrophils from both adults and neonates and present evidence showing that HSV-1 enhances apoptosis in neonatal, but not adult, neutrophils. HSV-1 enhanced the expression of both Fas and Fas ligand on the surface of neonatal neutrophils. Treatments with anti-Fas antibody and a Fas ligand inhibitor significantly reduced the induction of apoptosis by HSV-1. Using an ELISA assay, it was found that HSV-1 infection also leads to increased release of soluble FasL from HSV-1-infected neonatal neutrophils. Increased neonatal neutrophil apoptosis following HSV-1 infection may represent an important mechanism by which HSV-1 may diminish the antiviral response of neonatal neutrophils and might explain, at least in part, the severity of infections that are caused in newborns by this herpesvirus. (Pediatr Res 59: 7-12, 2006)

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Section: Discussionmentioning

confidence: 58%

Induction of Apoptosis by Herpes Simplex Virus-1 in Neonatal, But Not Adult, Neutrophils

et al. 2006

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“…Many previous studies have reported that serum sFas is elevated in patients with malignant disease [39,40]. Several studies have been performed showing an increased sFas serum concentration associated with a poor prognosis in patients suffering malignant disease [41,42]. Previous studies have also reported that the sFas levels were increased in the plasma from patients with inflammatory situations such as SIRS [23,32,42,43] and coronary bypass surgery [33].…”

Section: Discussionmentioning

confidence: 99%

Regulation of Fas-Mediated Apoptosis in Neutrophils after Surgery-Induced Acute Inflammation

Iwase

Kondo

Watanabe

et al. 2006

Journal of Surgical Research

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“…Dysregulation of the TNF signaling pathway has been implicated in the pathogenesis of many chronic liver diseases, including viral hepatitis, alcoholic liver disease and fulminant liver failure, while altered TNF signaling and increased activation of the TNF-mediated apoptotic pathways are associated with steatohepatitis and other hepatocellular abnormalities [8,9,10]. …”

Section: Role Of Cytokines In Liver Injurymentioning

confidence: 99%

“…Because the tissue-damaging mechanisms of cytokinesare closely related to their hepatocyte proliferation and liver regeneration function, it remains a challenge to selectively prevent the detrimental effects. More recent data point to the concept of ‘immune paralysis’ in patients with ACLF, which is defined as a reduction in monocyte human leukocyte antigen-R (HLA-DR) expression and therefore an impairment in LPS-stimulated proinflammatory cytokine production (IL-1, IL-6, IL-8, TNF-α) [10, 11]. The correlation of immune paralysis with the severity of ACLF has not been well established.…”

Section: Introductionmentioning

confidence: 99%

Role of Cytokines in the Pathophysiology of Acute-on-Chronic Liver Failure

Liu¹

2009

Blood Purif

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Background: This is the first ever decade which has witnessed the emergence of a highly lethal condition termed acute-on-chronic liver failure (ACLF), which today is the leading cause of death compared to acute and chronic liver failure. However, the complex pathophysiology of ACLF remains poorly understood. This article will attempt to summarize recent progress in the understanding of the mechanisms of cytokines in ACLF. Methods: The search terms used on PubMed were cytokines, liver injury, complications of liver disease, and hepatic progenitor cell. Results: Cytokines play a significant role in the pathophysiology of ACLF including hepatocellular death, extrahepatic complications and hepatocyte regeneration. The tissue-damaging mechanisms of cytokines are closely related to their hepatocyte proliferation and regeneration function. Conclusions: It remains a challenge to selectively prevent the detrimental effects of cytokines. To design interventions which selectively target the detrimental effects of cytokines, a detailed understanding of cytokines in the pathophysiology ACLF is critical.

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sFas and sFas Ligand and Pediatric Sepsis-Induced Multiple Organ Failure Syndrome

Cited by 52 publications

References 42 publications

Induction of Apoptosis by Herpes Simplex Virus-1 in Neonatal, But Not Adult, Neutrophils

Induction of Apoptosis by Herpes Simplex Virus-1 in Neonatal, But Not Adult, Neutrophils

Regulation of Fas-Mediated Apoptosis in Neutrophils after Surgery-Induced Acute Inflammation

Role of Cytokines in the Pathophysiology of Acute-on-Chronic Liver Failure

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