Analysis of the mechanisms involved in the stimulation of neutrophil apoptosis by tumour necrosis factor‐α

Salamone, Gabriela; Trevani, Analía Silvina; Martínez, Diego; Vermeulen, Mónica; Gamberale, Romina; Fernández-Calotti, Paula; Raiden, Silvina; Giordano, Mirta; Geffner, Jorge

doi:10.1111/j.1365-2567.2004.01973.x

Cited by 20 publications

(24 citation statements)

References 66 publications

(130 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Bid cleavage was not observed 66 and no changes in the mitochondrial transmembrane potential were detected, 105 no release of cytochrome c was measured, 66 and blocking caspase-9 by Z-LEHD-FMK did not significantly delay neutrophil apoptosis. 100,101 In keeping with this, neutrophils derived from bid knockout mice undergo TNF-a-induced apoptosis to the same extent as wild-type neutrophils. 66 On the other hand, changes in the mitochondrial shape from tubular structures to large, unstructured aggregates and Bax relocalization to mitochondria were reported in neutrophils upon TNF-a stimulation.…”

Section: Neutrophil Apoptosis Mediated By Death Receptorsmentioning

confidence: 60%

“…16,101 However, whether TNF-a stimulation results in caspase-8 activation is controversial. Although TNF-a stimulation was shown to increase caspase-8 processing 102 and activation 103 and blocking of caspase-8 by Z-IETD-FMK delayed TNF-a-induced neutrophil apoptosis, 100,101 other reports suggest that stimulation of TNF receptor does not involve caspase-8 processing or activation. 66,104 As compared with the uncertain role of caspase-8 upon TNF receptor ligation, caspase-3 processing and activation was reported unequivocally upon TNF-a stimulation.…”

Section: Neutrophil Apoptosis Mediated By Death Receptorsmentioning

confidence: 98%

“…84 The diverse outcome of TNF-a stimulation seems to depend on TNF-a concentrations, 97 duration of stimulation 98 and activation of co-stimulatory molecules, such as integrins. 97,99,100 TNF-a-induced neutrophil apoptosis is mediated by caspase activity, as blocking neutrophils with low concentrations of z-VAD-FMK inhibits cell death. 16,101 However, whether TNF-a stimulation results in caspase-8 activation is controversial.…”

Section: Neutrophil Apoptosis Mediated By Death Receptorsmentioning

confidence: 99%

See 2 more Smart Citations

Peculiarities of cell death mechanisms in neutrophils

2011

View full text Add to dashboard Cite

Analyses of neutrophil death mechanisms have revealed many similarities with other cell types; however, a few important molecular features make these cells unique executors of cell death mechanisms. For instance, in order to fight invading pathogens, neutrophils possess a potent machinery to produce reactive oxygen species (ROS), the phagocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Evidence is emerging that these ROS are crucial in the execution of most neutrophil cell death mechanisms. Likewise, neutrophils exhibit many diverse granules that are packed with cytotoxic mediators. Of those, cathepsins were recently shown to activate pro-apoptotic B-cell lymphoma-2 (Bcl-2) family members and caspases, thus acting on apoptosis regulators. Moreover, neutrophils have few mitochondria, which hardly participate in ATP synthesis, as neutrophils gain energy from glycolysis. In spite of relatively low levels of cytochrome c in these cells, the mitochondrial death pathway is functional. In addition to these pecularities defining neutrophil death pathways, neutrophils are terminally differentiated cells, hence they do not divide but undergo apoptosis shortly after maturation. The initial trigger of this spontaneous apoptosis remains to be determined, but may result from low transcription and translation activities in mature neutrophils. Due to the unique biological characteristics of neutrophils, pharmacological intervention of inflammation has revealed unexpected and sometimes disappointing results when neutrophils were among the prime target cells during therapy. In this study, we review the current and emerging models of neutrophil cell death mechanisms with a focus on neutrophil peculiarities.

show abstract

Section: Neutrophil Apoptosis Mediated By Death Receptorsmentioning

confidence: 60%

Section: Neutrophil Apoptosis Mediated By Death Receptorsmentioning

confidence: 98%

Section: Neutrophil Apoptosis Mediated By Death Receptorsmentioning

confidence: 99%

See 1 more Smart Citation

Peculiarities of cell death mechanisms in neutrophils

2011

View full text Add to dashboard Cite

show abstract

“…Therefore, in neutrophils, a prolonged increase in intracellular Ca +2 may stimulate cytokine release and the accumulation and activation of phagocytes. Cytokines released by chronically activated phagocytes can also trigger apoptosis [29], formation of reactive oxygen species [30] and increase in intracellular Ca +2 , for example. The latter can prime the cells for the release of more cytokine [31].…”

Section: Discussionmentioning

confidence: 99%

Neutrophils and monocytes as potentially important sources of proinflammatory cytokines in diabetes

Hatanaka

Monteagudo

Marrocos

et al. 2006

Clinical and Experimental Immunology

174

137

View full text Add to dashboard Cite

SummaryNeutrophils and monocytes play a central role in host defence. The invading leucocytes are capable of synthesizing and releasing a variety of proinflammatory mediators including cytokines. Given the importance of cytokines in the progression of chronic and acute inflammatory processes, we aimed to ascertain whether the release of interleukin (IL)-8, IL-1b, tumour necrosis factor (TNF)-a and IL-1ra of neutrophils and monocytes was modified in diabetes. To this end, we measured the release of cytokines in suspensions of cell culture in basal and lipopolysaccharide (LPS)-stimulated conditions. In basal conditions, neutrophils of diabetics release 1·6, 3·2, 1·9 and 1·9-fold higher amounts of IL-8, IL-1b, TNF-a and IL-1ra, respectively, than do healthy controls. Under our experimental conditions, this effect was more evident for neutrophils than for monocytes. Incremental cytokine production was also found to occur when neutrophils were stimulated with LPS. IL-8, IL-1b and TNF-a increased, respectively, by 4·0, 1·7 and 2·8-fold. Although the effect was more marked for neutrophils, monocytes showed a tendency for increased cytokine production. The discovery of this increase in cytokines released by the neutrophils of diabetics contributes towards a clearer understanding of other deficiencies described for neutrophils in diabetes, such as the migration of neutrophils to inflammatory sites, phagocytes, release of lytic proteases, production of reactive oxygen species and apoptosis. The excessive production of cytokines may lead to inappropriate activation and tissue injury and even to increased susceptibility to invasive microorganisms. Thus, the increased responsiveness of neutrophils of diabetics demonstrated in this study may be considered part of the scenario of diabetes physiopathology.

show abstract

“…specific cleavage of many key cellular proteins during apoptosis (20,22,26). Furthermore, several pieces of evidence suggested that using caspase inhibitors reduces TNF-a-mediated liver injury (27).…”

Section: Fig 4 Effect Ofpd On the Changes Oficam Ecamprotein Exprementioning

confidence: 99%

Polydatin Protects against Lipopolysaccharide-Induced Fulminant Hepatic Failure in D-Galactosamine-Sensitized Mice

Gong

Jiang

et al. 2012

Int J Immunopathol Pharmacol

View full text Add to dashboard Cite

The first two authors contributed equally to the manuscript Fulminant hepatic failure (FHF) is a devastating clinical syndrome with extremely poor prognosis and high mortality. Therefore, better treatment is urgently needed. Polydatin (PD), a traditional antiinflammatory drug, has been described to protect against liver inj ury induced by certain hepatotoxins. The present study investigated the protective effect of PD against lipopolysaccharide (LPS)ill-galactosamine (D-GaIN)-induced FHF in mice and the underlying mechanism. Mice were pretreated with an increasing dose of PD (10, 30, and 100 mglkg), following LPSID-GaIN challenge. The liver injury was assessed biochemically and histologically. We found that PD exerted a protective effect on LPSID-GaIN-induced FHF as evidenced by reducing sera alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, diminishing liver histopathological injury, and lowering mortality in a dose-dependent manner. In addition, pretreatment mice with PD dose-dependently suppressed tumor necrosis factor-a (TNF-a) production, myeloperoxidase (MPO) activity, intercellular adhesion molecule-l (ICAM-l) and endothelial cell adhesion molecule-l (ECAM-l) expression, caspase-3 activation, and transcription factor nuclear factor-kappa B(NF-KB) activity induced by LPS. These results suggested that PD could effectively protect from LPSID-GaIN-induced FHF and the protective effect afforded by PD probably contributed to reduce TNF-a production via inhibiting NF-kB activation.

show abstract

Analysis of the mechanisms involved in the stimulation of neutrophil apoptosis by tumour necrosis factor‐α

Cited by 20 publications

References 66 publications

Peculiarities of cell death mechanisms in neutrophils

Peculiarities of cell death mechanisms in neutrophils

Neutrophils and monocytes as potentially important sources of proinflammatory cytokines in diabetes

Polydatin Protects against Lipopolysaccharide-Induced Fulminant Hepatic Failure in D-Galactosamine-Sensitized Mice

Contact Info

Product

Resources

About