<scp>NETosis</scp>and<scp>ETosis</scp>: Incompletely Understood Types of Granulocyte Death and their Proposed Adaptive Benefits and Costs

Radic, Marko

doi:10.1002/9781119432463.ch24

Cited by 3 publications

(2 citation statements)

References 142 publications

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“…It is important to highlight that other granulocytes are also capable of producing ETs and lead to cell death [ 212 ]. Therefore, it is still a topic of discussion among researchers on whether the correct term to adopt is NETosis or ETosis, since NETosis would be a specialized form of ETosis [ 213 ].…”

Section: Cell Deathmentioning

confidence: 99%

Unraveling Cell Death Pathways during Malaria Infection: What Do We Know So Far?

Sena-dos-Santos

Braga-da-Silva

Marques

et al. 2021

Cells

101

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Malaria is a parasitic disease (caused by different Plasmodium species) that affects millions of people worldwide. The lack of effective malaria drugs and a vaccine contributes to this disease, continuing to cause major public health and socioeconomic problems, especially in low-income countries. Cell death is implicated in malaria immune responses by eliminating infected cells, but it can also provoke an intense inflammatory response and lead to severe malaria outcomes. The study of the pathophysiological role of cell death in malaria in mammalians is key to understanding the parasite–host interactions and design prophylactic and therapeutic strategies for malaria. In this work, we review malaria-triggered cell death pathways (apoptosis, autophagy, necrosis, pyroptosis, NETosis, and ferroptosis) and we discuss their potential role in the development of new approaches for human malaria therapies.

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Section: Cell Deathmentioning

confidence: 99%

Unraveling Cell Death Pathways during Malaria Infection: What Do We Know So Far?

Sena-dos-Santos

Braga-da-Silva

Marques

et al. 2021

Cells

101

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“…They are released into the bloodstream mainly through cell death mechanisms, such as apoptosis or necrosis, and through innate immune processes such as ETosis [ 48 ], a process which requires the nuclear citrullination of H3 [ 49 , 50 ]. ETosis modulates the overactivation of the immune system during sepsis; hence, it would be expected to find a high amount of citrullinated histones (especially H3cit) into the bloodstream in the first stages of sepsis, just when the innate immunity is occurring [ 51 , 52 ]. However, we found that, despite levels of circulating histones remaining elevated during the stay of patients in the ICU, the levels of circulating H3cit decreased along the septic process.…”

Section: Discussionmentioning

confidence: 99%

Histone Citrullination Mediates a Protective Role in Endothelium and Modulates Inflammation

Osca-Verdegal

Beltrán-García²,

Paes

et al. 2022

Cells

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NETosis is a key host immune process against a pathogenic infection during innate immune activation, consisting of a neutrophil “explosion” and, consequently, NET formation, containing mainly DNA, histones, and other nuclear proteins. During sepsis, an exacerbated immune host response to an infection occurs, activating the innate immunity and NETosis events, which requires histone H3 citrullination. Our group compared the circulating histone levels with those citrullinated H3 levels in plasma samples of septic patients. In addition, we demonstrated that citrullinated histones were less cytotoxic for endothelial cells than histones without this post-translational modification. Citrullinated histones did not affect cell viability and did not activate oxidative stress. Nevertheless, citrullinated histones induced an inflammatory response, as well as regulatory endothelial mechanisms. Furthermore, septic patients showed elevated levels of circulating citrullinated histone H3, indicating that the histone citrullination is produced during the first stages of sepsis, probably due to the NETosis process.

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Comprehensive review of lipocalin 2-mediated effects in lung inflammation

Guardado

Ojeda-Juárez

Kaul

et al. 2021

American Journal of Physiology-Lung Cellular and Molecular Phys

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Lipocalin-2 (LCN2) is an inflammatory mediator best known for its role as an innate acute-phase protein. LCN2 mediates the innate immune response to pathogens by sequestering iron, thereby inhibiting pathogen growth. Though LCN2 and its bacteriostatic properties are well studied, other LCN2 functions in the immune response to inflammatory stimuli are less well understood, such as its role as a chemoattractant and involvement in the regulation of cell migration and apoptosis. In the lungs, most studies thus far investigating the role of LCN2 in the immune response have looked at pathogenic inflammatory stimuli. Here, we compile data that explore the role of LCN2 in the immune response to various inflammatory stimuli in an effort to differentiate between protective versus detrimental roles of LCN2.

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NETosisandETosis: Incompletely Understood Types of Granulocyte Death and their Proposed Adaptive Benefits and Costs

Cited by 3 publications

References 142 publications

Unraveling Cell Death Pathways during Malaria Infection: What Do We Know So Far?

Unraveling Cell Death Pathways during Malaria Infection: What Do We Know So Far?

Histone Citrullination Mediates a Protective Role in Endothelium and Modulates Inflammation

Comprehensive review of lipocalin 2-mediated effects in lung inflammation

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