Constitutive neutrophil apoptosis: Mechanisms and regulation

Luo, Hongbo; Loison, Fabien

doi:10.1002/ajh.21078

Cited by 258 publications

(295 citation statements)

References 147 publications

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“…Neutrophil contents are potentially harmful to the host and the release and activation of their microbicidal arsenal is strongly controlled by strict regulation of degranulation and superoxide production, as well as by regulation of their life span and recruitment into tissues. In the absence of immunological challenge, differentiated neutrophils are committed to undergo caspase-dependent apoptosis within 24 to 48 h after their emigration from the bone marrow [1]. During infection, the rate of programmed cell death can be further modulated by various exogenous and endogenous stimuli that either extend or shorten the neutrophil life span [2].…”

Section: Introductionmentioning

confidence: 99%

Neutrophil extracellular trap cell death requires both autophagy and superoxide generation

et al. 2010

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Neutrophil extracellular traps (NETs) are extracellular chromatin structures that can trap and degrade microbes. They arise from neutrophils that have activated a cell death program called NET cell death, or NETosis. Activation of NETosis has been shown to involve NADPH oxidase activity, disintegration of the nuclear envelope and most granule membranes, decondensation of nuclear chromatin and formation of NETs. We report that in phorbol myristate acetate (PMA)-stimulated neutrophils, intracellular chromatin decondensation and NET formation follow autophagy and superoxide production, both of which are required to mediate PMA-induced NETosis and occur independently of each other. Neutrophils from patients with chronic granulomatous disease, which lack NADPH oxidase activity, still exhibit PMA-induced autophagy. Conversely, PMA-induced NADPH oxidase activity is not affected by pharmacological inhibition of autophagy. Interestingly, inhibition of either autophagy or NADPH oxidase prevents intracellular chromatin decondensation, which is essential for NETosis and NET formation, and results in cell death characterized by hallmarks of apoptosis. These results indicate that apoptosis might function as a backup program for NETosis when autophagy or NADPH oxidase activity is prevented.

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Section: Introductionmentioning

confidence: 99%

Neutrophil extracellular trap cell death requires both autophagy and superoxide generation

et al. 2010

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“…Phagocytic cells produce superoxide anions and hydrogen peroxide radicals as second messengers and as part of the degradation process of pathogens. However, if radical production becomes excessive it will be toxic for the phagocyte as well as for the surrounding cells and tissue [43].…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have shown that caspase-3 is not only involved in ROS-induced apoptosis, but also has been suggested to become activated by ROS itself [43,51,52].…”

Section: Discussionmentioning

confidence: 99%

In vivo and in vitro evaluation of hydroxyapatite nanoparticle morphology on the acute inflammatory response

et al. 2016

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In vivo and in vitro evaluation of hydroxyapatite nanoparticle morphology on the acute inflammatory response. AbstractBiomedical implants have been widely used in bone repair applications. However, nanosized degradation products from these implants could elicit an inflammatory reaction, which may lead to implant failure. It is well known that the size, chemistry, and charge of these nanoparticles can modulate this response, but little is known regarding the role that the particle's morphology plays in inducing inflammation. The present study aims to investigate the effect of hydroxyapatite nanoparticle (HANPs) morphology on inflammation, in-vitro and in-vivo. Four distinct HANP morphologies were fabricated and characterized: long rods, dots, sheets, and fibers. Primary human polymorphonuclear cells (PMNCs), mononuclear cells (MNCs), and human dermal fibroblasts (hDFs) were exposed to HANPs and alterations in cell viability, morphology, apoptotic activity, and reactive oxygen species (ROS) production were evaluated, in vitro. PMNCs and hDFs experienced a 2-fold decrease in viability following exposure to fibers, while MNC viability decreased 5-fold after treatment with the dots. Additionally, the fibers stimulated an elevated ROS response in both PMNCs and MNCs, and the largest apoptotic behavior for all cell types. Furthermore, exposure to fibers and dots resulted in greater capsule thickness when implanted subcutaneously in mice. Collectively, these results suggest that nanoparticle morphology can significantly impact the inflammatory response.

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“…After the completion of task, apoptosis of the inflammatory cells and their subsequent clearance (efferocytosis) by macrophages are key mechanisms orchestrating successful resolution of inflammation (Luo and Loison 2008;Michlewska et al 2009;Dalli and Serhan 2012). It has been well established that neutrophil accumulation frequently occurs at the site of snakebite as part of the inflammatory response to envenoming (Wei et al 2010).…”

Section: Discussionmentioning

confidence: 99%

“…Several snake venom disintegrins, a group of cysteine rich proteins have been shown to induce the neutrophil chemotaxis. After the completion of the task the activated neutrophils are removed from the system through apoptosis and phagocytosed by macrophages resulting in resolution of inflammation (Coelho et al 2004;Luo and Loison 2008). However, if neutrophil death occurs before their function, the number of functional neutrophils in the target site will get reduced.…”

Section: Introductionmentioning

confidence: 99%

Propensity of crocin to offset Vipera russelli venom induced oxidative stress mediated neutrophil apoptosis: a biochemical insight

et al. 2014

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Viper envenomation results in inflammation at the bitten site as well as target organs. Neutrophils and other polymorphonuclear leukocytes execute inflammation resolving mechanism and will undergo apoptosis after completing the task. However, the target specific toxins induce neutrophil apoptosis at the bitten site and in circulation prior to their function, thus reducing their number. Circulating activated neutrophils are major source of inflammatory cytokines and leakage of reactive oxygen species (ROS)/other toxic intermediates resulting in aggravation of inflammatory response at the bitten/target site. Therefore, neutralization of venom induced neutrophil apoptosis reduces inflammation besides increasing the functional neutrophil population. Therefore, the present study investigates the venom induced perturbances in isolated human neutrophils and its neutralization by crocin (Crocus sativus) a potent antioxidant carotenoid. Human neutrophils on treatment with venom resulted in altered ROS generation, intracellular Ca 2? mobilization, mitochondrial membrane depolarization, cyt-c translocation, caspase activation, phosphatidylserine externalization and DNA damage. On the other hand significant protection against oxidative stress and apoptosis were evidenced in crocin pre-treated groups. In conclusion the viper venom induces neutrophil apoptosis and results in aggravation of inflammation and tissue damage. The present study demands the necessity of an auxiliary therapy in addition to antivenin therapy to treat secondary/overlooked complications of envenomation.

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Constitutive neutrophil apoptosis: Mechanisms and regulation

Cited by 258 publications

References 147 publications

Neutrophil extracellular trap cell death requires both autophagy and superoxide generation

Neutrophil extracellular trap cell death requires both autophagy and superoxide generation

In vivo and in vitro evaluation of hydroxyapatite nanoparticle morphology on the acute inflammatory response

Propensity of crocin to offset Vipera russelli venom induced oxidative stress mediated neutrophil apoptosis: a biochemical insight

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