Induction of Bim and Bid gene expression during accelerated apoptosis in severe sepsis

Weber, Stefan; Schewe, Jens-Christian; Lehmann, Lutz; Müller, Stefan; Book, Malte; Klaschik, Sven; Hoeft, Andreas; Stüber, Frank

doi:10.1186/cc7088

Cited by 75 publications

(56 citation statements)

References 50 publications

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“…Our current study strongly suggests that lymphocytes (and not monocytes) drive this pro-apoptotic gene expression profile in unseparated circulating mononuclear cells. In accordance, BCL2 protein expression was reported to be downregulated in CD4+ T cells of patients with sepsis [22] .…”

Section: Discussionsupporting

confidence: 52%

“…A very recent study, using microarrays with 1 50,000 transcripts, showed enhanced activation of genes involved in apoptosis in peripheral blood mononuclear cells of sepsis patients [21] . Moreover, in a separate study, sepsis patients displayed gene expression profiles in whole-blood leukocytes compatible with increased apoptosis [22] . These investigations did not provide insight regarding the contribution of apoptotic mediators in purified leukocyte subsets.…”

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confidence: 91%

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Gene Expression Profiling of Apoptosis Regulators in Patients with Sepsis

et al. 2010

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Introduction: Sepsis is associated with a dysregulation of apoptosis in immune cells, which has been implicated in both immunosuppression and multiple organ failure. We describe the expression profiles of genes encoding key regulators of apoptosis in highly purified monocytes, granulocytes and CD4+ T lymphocytes. Methods: Sixteen patients with sepsis were recruited from the intensive care unit and were compared with 24 healthy controls. RNA was isolated from highly purified monocyte, granulocyte and CD4+ T-lymphocyte populations. Gene expression profiles were determined using multiplex ligation-dependent probe amplification for the simultaneous detection of 30 pro- and anti-apoptotic target genes. Results: Relative to healthy controls, patients with sepsis showed increased transcription of both pro- and anti-apoptotic genes in peripheral blood leukocytes. Specific monocyte, granulocyte and CD4+ T-lymphocyte mRNA profiles were identified. Anti-apoptotic profiles were found in monocytes and granulocytes, while CD4+ T lymphocytes displayed a foremost pro-apoptotic mRNA profile. Conclusions: These data indicate that in patients with sepsis, the alterations in apoptosis of circulating leukocytes occur in a cell-specific manner.

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Section: Discussionsupporting

confidence: 52%

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confidence: 91%

Gene Expression Profiling of Apoptosis Regulators in Patients with Sepsis

et al. 2010

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“…Interestingly, Weber and colleagues have recently described a massive upregulation of proapoptotic factors in circulating blood cells from patients suffering from severe sepsis (40). They further concluded that the proapoptotic pattern of gene expression must be generated by lymphocytes, displaying increased apoptosis in sepsis, rather than neutrophils with prolonged life span (40). However, this work demonstrates that the gene expression of most pro apoptotic genes such as Bax, Bad, and Bid is also upregulated in neutrophils after major trauma showing prolonged life span.…”

Section: Discussionmentioning

confidence: 99%

Molecular Mechanisms Underlying Delayed Apoptosis in Neutrophils from Multiple Trauma Patients with and without Sepsis

Paunel-Görgülü

Kirichevska

Lögters

et al. 2011

Mol Med

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“…Perhaps, if the comparisons were restricted to a particular cell class, such as circulating lymphocytes or monocytes, a much better correlation of the genomic response between mice and humans might have existed. In this regard, the dramatic upregulation in mouse lymphocytes of the genes encoding pro-apoptotic B cell lymphoma 2 (BCL-2) family members and downregulation of genes encoding anti-apoptotic BCL-2 family members has also been documented in lymphocytes from patients with sepsis 170,171 . The significance of this correlation for a particular class of genes in mice and humans is highlighted by the fact that apoptosis is a key pathogenic mechanism in sepsis.…”

Section: Figurementioning

confidence: 99%

Sepsis-induced immunosuppression: from cellular dysfunctions to immunotherapy

2013

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Sepsis — severe life-threatening infection with organ dysfunction — initiates a complex interplay of host pro- and anti-inflammatory processes. In a real sense, sepsis can be considered a race to the death between the pathogens and the host immune system. It is the proper balance between the often competing pro- and anti-inflammatory pathways that determines the fate of the individual. Although the field of sepsis research has witnessed the failure of many highly-touted clinical trials, a better understanding of the pathophysiological basis of the disorder and the mechanisms responsible for the associated pro- and anti-inflammatory responses is leading to a novel approach to treat this highly lethal condition. Biomarker-guided immunotherapy administered to patients at the proper immune phase of sepsis represents a potential major advance in the treatment of sepsis and more broadly in the field of infectious disease.

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Induction of Bim and Bid gene expression during accelerated apoptosis in severe sepsis

Cited by 75 publications

References 50 publications

Gene Expression Profiling of Apoptosis Regulators in Patients with Sepsis

Gene Expression Profiling of Apoptosis Regulators in Patients with Sepsis

Molecular Mechanisms Underlying Delayed Apoptosis in Neutrophils from Multiple Trauma Patients with and without Sepsis

Sepsis-induced immunosuppression: from cellular dysfunctions to immunotherapy

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