Peculiarities of cell death mechanisms in neutrophils.
Barbara Geering,Hans-Uwe Simon +1 more
Reads0
Chats0
TLDR
The current and emerging models of neutrophil cell death mechanisms are reviewed with a focus on neutrophils peculiarities, including mitochondrial death pathway, and pharmacological intervention of inflammation.Abstract:
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.read more
Citations
More filters
Journal ArticleDOI
Neutrophil Necroptosis Is Triggered by Ligation of Adhesion Molecules following GM-CSF Priming
TL;DR: It is reported that human neutrophils undergo necroptosis after exposure to GM-CSF followed by the ligation of adhesion receptors such as CD44, CD11b, CD18, or CD15, and it is shown that MLKL undergoes phosphorylation in neutrophil in vivo under inflammatory conditions, implying that targeting adhesion molecules could be beneficial for preventing exacerbation of disease in the neutrophilic inflammatory response.
Journal ArticleDOI
From neutrophil extracellular traps release to thrombosis: an overshooting host-defense mechanism?
Julian I. Borissoff,H. ten Cate +1 more
TL;DR: Scientific evidence suggests that activation of blood coagulation, leading to subsequent fibrin deposition at the sites of inflammation, is an additional protective mechanism serving against microbial dissemination, and neutrophil hyperresponsiveness may trigger an overreactive host defense response over time.
Targeting Neutrophil Apoptosis for Enhancing the Resolution ofInflammation
TL;DR: In this paper, the potential of therapeutic induction of leukocyte cell death for moistening neutrophil-mediated tissue injury and inflammation underlying a spread of diseases was discussed, lightness of lightness the potential for therapeutic induction for leukocytes cell death.
Journal ArticleDOI
Identification of NCF2/p67phox as a novel p53 target gene.
TL;DR: Insight is provided into the redox-sensitive signaling mechanism that mediates cell survival involving p53 and its novel target NCF2/p67phox, suggesting a protective function of Nox2-generated ROS in cells against apoptosis.
Journal ArticleDOI
Silver nanoparticles rapidly induce atypical human neutrophil cell death by a process involving inflammatory caspases and reactive oxygen species and induce neutrophil extracellular traps release upon cell adhesion.
TL;DR: In this paper, the effect of nanoparticles on neutrophil apoptosis was evaluated using transmission electronic microscopy and it was shown that AgNPs rapidly penetrate inside neutrophils and induce atypical cell death.
References
More filters
Journal ArticleDOI
Neutrophil extracellular traps kill bacteria
Volker Brinkmann,Ulrike Reichard,Christian Goosmann,Beatrix Fauler,Yvonne Uhlemann,David S. Weiss,Yvette Weinrauch,Yvette Weinrauch,Arturo Zychlinsky +8 more
TL;DR: It is described that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria, which degrade virulence factors and kill bacteria.
Journal ArticleDOI
Classification of cell death: recommendations of the Nomenclature Committee on Cell Death
Guido Kroemer,Guido Kroemer,Guido Kroemer,Lorenzo Galluzzi,Lorenzo Galluzzi,Lorenzo Galluzzi,Peter Vandenabeele,John M. Abrams,Emad S. Alnemri,Eric H. Baehrecke,Mikhail V. Blagosklonny,Wafik S. El-Deiry,Pierre Golstein,Pierre Golstein,Douglas R. Green,Michael O. Hengartner,Richard A. Knight,Sharad Kumar,Stuart A. Lipton,Stuart A. Lipton,Stuart A. Lipton,Walter Malorni,Gabriel Núñez,Marcus E. Peter,Juerg Tschopp,Junying Yuan,Mauro Piacentini,Boris Zhivotovsky,Gerry Melino,Gerry Melino +29 more
TL;DR: This study details the 2009 recommendations of the NCCD on the use of cell death-related terminology including ‘entosis’, ‘mitotic catastrophe”,’ ‘necrosis‚ ‘necroptosis‚’ and ‘pyroptotic’.
Journal ArticleDOI
Role of reactive oxygen species (ROS) in apoptosis induction
TL;DR: The role of ROS in the regulation of apoptosis, especially in inflammatory cells, is focused on, with particular attention to mitochondria.
Journal ArticleDOI
Novel cell death program leads to neutrophil extracellular traps
Tobias A. Fuchs,Ulrike Abu Abed,Christian Goosmann,Robert Hurwitz,Ilka Schulze,Volker Wahn,Yvette Weinrauch,Volker Brinkmann,Arturo Zychlinsky +8 more
TL;DR: This novel ROS-dependent death allows neutrophils to fulfill their antimicrobial function, even beyond their lifespan.
Journal ArticleDOI
Chronic granulomatous disease. Report on a national registry of 368 patients.
Jerry A. Winkelstein,Mary C. Marino,Richard B. Johnston,John Boyle,John T. Curnutte,John I. Gallin,Harry L. Malech,S.M. Holland,Hans D. Ochs,Paul G. Quie,Rebecca H. Buckley,Charles B. Foster,S. J. Chanock,Howard B. Dickler +13 more
TL;DR: A registry of United States residents with chronic granulomatous disease (CGD) was established in 1993 in order to estimate the minimum incidence of this uncommon primary immunodeficiency disease and characterize its epidemiologic and clinical features.