Induction of Neutrophil Extracellular DNA Lattices by Placental Microparticles and IL-8 and Their Presence in Preeclampsia

Gupta, Anurag; Harmatz, Paul; Holzgreve, Wolfgang; Gebhardt, Stefan; Hahn, Sinuhe

doi:10.1016/j.humimm.2005.11.003

Cited by 352 publications

(351 citation statements)

References 25 publications

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“…NETs have been visualized in vivo under diverse settings, such as in human appendicitis, lupine Shigella-induced dysentery (2), bovine mastitis (24), human preeclampsia (25,26), and in the blood of Plasmodium falciparum-infected children (27). Based on our findings that these lattices occur in patients' lesions, and NETs trap and kill Leishmania, we could envisage that NETs could be relevant to control the parasite burden and modulate the immune response through the components released together with the lattices.…”

Section: Discussionmentioning

confidence: 99%

Leishmania amazonensispromastigotes induce and are killed by neutrophil extracellular traps

Guimarães-Costa

Nascimento²,

Froment³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

484

429

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Neutrophils are short-lived leukocytes that die by apoptosis, necrosis, and NETosis. Upon death by NETosis, neutrophils release fibrous traps of DNA, histones, and granule proteins named neutrophil extracellular traps (NETs), which can kill bacteria and fungi. Inoculation of the protozoan Leishmania into the mammalian skin causes local inflammation with neutrophil recruitment. Here, we investigated the release of NETs by human neutrophils upon their interaction with Leishmania parasites and NETs' ability to kill this protozoan. The NET constituents DNA, elastase, and histones were detected in traps associated to promastigotes by immunofluorescence. Electron microscopy revealed that Leishmania was ensnared by NETs released by neutrophils. Moreover, Leishmania and its surface lipophosphoglycan induced NET release by neutrophils in a parasite number-and dose-dependent manner. Disruption of NETs by DNase treatment during Leishmania-neutrophil interaction increased parasite survival, evidencing NETs' leishmanicidal effect. Leishmania killing was also elicited by NET-rich supernatants from phorbol 12-myristate 13-acetate-activated neutrophils. Immunoneutralization of histone during Leishmania-neutrophil interaction partially reverted Leishmania killing, and purified histone killed the parasites. Meshes composed of DNA and elastase were evidenced in biopsies of human cutaneous leishmaniasis. NET is an innate response that might contribute to diminish parasite burden in the Leishmania inoculation site.histone ͉ protozoa ͉ trypanosomatid

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Section: Discussionmentioning

confidence: 99%

Leishmania amazonensispromastigotes induce and are killed by neutrophil extracellular traps

Guimarães-Costa

Nascimento²,

Froment³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

484

429

View full text Add to dashboard Cite

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“…One of the main SASP components is IL-8, which is strongly up-regulated in fused senescent cells and is essential for normal placental function (Dame and Juul 2000;Gupta et al 2005). Other SASP cytokines secreted from the fused cells, such as CCL5, attract specific noncytotoxic maternal NK cells that play an important role in maintenance of the placenta (Hanna et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Cell fusion induced by ERVWE1 or measles virus causes cellular senescence

et al. 2013

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Cellular senescence limits proliferation of potentially detrimental cells, preventing tumorigenesis and restricting tissue damage. However, the function of senescence in nonpathological conditions is unknown. We found that the human placental syncytiotrophoblast exhibited the phenotype and expressed molecular markers of cellular senescence. During embryonic development, ERVWE1-mediated cell fusion results in formation of the syncytiotrophoblast, which serves as the maternal/fetal interface at the placenta. Expression of ERVWE1 caused cell fusion in normal and cancer cells, leading to formation of hyperploid syncytia exhibiting features of cellular senescence. Infection by the measles virus, which leads to cell fusion, also induced cellular senescence in normal and cancer cells. The fused cells activated the main molecular pathways of senescence, the p53-and p16-pRbdependent pathways; the senescence-associated secretory phenotype; and immune surveillance-related proteins. Thus, fusion-induced senescence might be needed for proper syncytiotrophoblast function during embryonic development, and reuse of this senescence program later in life protects against pathological expression of endogenous fusogens and fusogenic viral infections.

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“…12,13 (4) The pro-inflammatory stimuli LPS and IL-8, which were reported to induce NETosis, 4,60 are unable to trigger NADPH oxidase activity, but only sensitize the cells to an oxidative burst. 61 This may explain why only some groups observed NET formation in response to LPS and IL-8, 4,60 while others observed a delay in neutrophil apoptosis, 2,62 but no NET formation.…”

Section: Net Release By Dying Cells (Netosis)mentioning

confidence: 99%

“…61 This may explain why only some groups observed NET formation in response to LPS and IL-8, 4,60 while others observed a delay in neutrophil apoptosis, 2,62 but no NET formation. 12,36,63 Serine proteases are also detected in neutrophil-derived NETs (Supplementary Table 1).…”

Section: Net Release By Dying Cells (Netosis)mentioning

confidence: 99%

Dying for a cause: NETosis, mechanisms behind an antimicrobial cell death modality

et al. 2011

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Neutrophil extracellular traps (NETs) are chromatin structures loaded with antimicrobial molecules. They can trap and kill various bacterial, fungal and protozoal pathogens, and their release is one of the first lines of defense against pathogens. In vivo, NETs are released during a form of pathogen-induced cell death, which was recently named NETosis. Ex vivo, both dead and viable neutrophils can be stimulated to release NETs composed of either nuclear or mitochondrial chromatin, respectively. In certain pathological conditions, NETs are associated with severe tissue damage or certain auto-immune diseases. This review describes the recent progress made in the identification of the mechanisms involved in NETosis and discusses its interplay with autophagy and apoptosis. Cell Death and Differentiation (2011) 18, 581-588; doi:10.1038/cdd.2011.1; published online 4 February 2011Neutrophils have an essential role in innate immunity and are the first cells recruited to the site of infection.1 Human neutrophils are the most abundant leukocytes. They have a very short lifespan, and neutrophil homeostasis is maintained by continuous release of many neutrophils from the bone marrow. Accelerated neutrophil death decreases neutrophil counts (neutropenia) and increases susceptibility to infection. In turn, delayed neutrophil death increases neutrophil counts (neutrophilia) and intensifies innate defenses, possibly promoting chronic inflammation.2 Neutrophils perform their function by engulfing microorganisms or opsonized particles and degrading them by various molecules, and also release lytic enzymes that destroy extracellular pathogens.3 Moreover, they release structures called neutrophil extracellular traps (NETs) that can trap and kill microbes. 4 The neutrophil lifespan constitutes a sensitive balance between their function as effecter cells and their potential to inflict tissue damage. In the absence of inflammatory stimuli, neutrophils continuously undergo apoptosis within 24-48 h both in vivo and in cell culture. The large amounts of superoxide produced by the membrane-associated NADPH oxidase in neutrophils have a central role in the destruction of invading pathogens as well as in the resolution of inflammation. [5][6][7][8][9] Congenital defects that prevent NADPH oxidase activity result in chronic granulomatous disease (CGD), which is characterized by exaggerated immune responses 10 and recurrent life-threatening infections by a narrow set of microorganisms. 11 We recently found that formation of NETs by activated neutrophils requires not only NADPH-oxidasemediated superoxide production, but also autophagy. 12In this review, we present an overview of the main biochemical and morphological features observed during neutrophil activation and discuss in more detail the contribution of NADPH oxidase, histone citrullination, intracellular calcium levels and autophagy to chromatin decondensation and NET formation. Release of Extracellular TrapsIn 2004, the group of Brinkman and Zychlinsky was the first to report the rele...

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Induction of Neutrophil Extracellular DNA Lattices by Placental Microparticles and IL-8 and Their Presence in Preeclampsia

Cited by 352 publications

References 25 publications

Leishmania amazonensispromastigotes induce and are killed by neutrophil extracellular traps

Leishmania amazonensispromastigotes induce and are killed by neutrophil extracellular traps

Cell fusion induced by ERVWE1 or measles virus causes cellular senescence

Dying for a cause: NETosis, mechanisms behind an antimicrobial cell death modality

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