Instructive influences of phagocytic clearance of dying cells on neutrophil extracellular trap generation

Manfredi, Angelo A.; Covino, Cesare; Rovere‐Querini, Patrizia; Maugeri, Norma

doi:10.1111/cei.12320

Cited by 36 publications

(33 citation statements)

References 31 publications

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“…We observed that the concurrence of necrotic cells and NETosis leads to the entrapment of the dead cells. A recent report on NETosis induced by apoptotic cells in vitro also supports the link between cell death and NETosis (49). …”

Section: Discussionmentioning

confidence: 56%

Oxidative Burst-Dependent NETosis Is Implicated in the Resolution of Necrosis-Associated Sterile Inflammation

et al. 2016

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Necrosis is associated with a profound inflammatory response. The regulation of necrosis-associated inflammation, particularly the mechanisms responsible for resolution of inflammation is incompletely characterized. Nanoparticles are known to induce plasma membrane damage and necrosis followed by sterile inflammation. We observed that injection of metabolically inert nanodiamonds resulted in paw edema in WT and Ncf1** mice. However, while inflammation quickly resolved in WT mice, it persisted over several weeks in Ncf1** mice indicating failure of resolution of inflammation. Mechanistically, NOX2-dependent reactive oxygen species (ROS) production and formation of neutrophil extracellular traps were essential for the resolution of necrosis-induced inflammation: hence, by evaluating the fate of the particles at the site of inflammation, we observed that Ncf1** mice deficient in NADPH-dependent ROS failed to generate granulation tissue therefore being unable to trap the nanodiamonds. These data suggest that NOX2-dependent NETosis is crucial for preventing the chronification of the inflammatory response to tissue necrosis by forming NETosis-dependent barriers between the necrotic and healthy surrounding tissue.

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Section: Discussionmentioning

confidence: 56%

Oxidative Burst-Dependent NETosis Is Implicated in the Resolution of Necrosis-Associated Sterile Inflammation

et al. 2016

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“…45 Apoptosis has been described in inflammatory myopathies, 46,47 at least in some cases as a result of the cytotoxic action of T lymphocytes. Finally, the generation of neutrophil extracellular traps (NETs), an event strictly associated with the activation of autophagy pathway in inflammatory leukocytes 48 and modulated by the recognition of apoptotic cells, 49 has been described in the muscle upon ischemia-reperfusion injury. 50 Further studies will evaluate the relevance of NET contribution to muscle remodeling during autoimmune diseases and in homeostatic conditions.…”

Section: Unique Immune Privileges Of the Skeletal Musclementioning

confidence: 99%

Cell death, clearance and immunity in the skeletal muscle

et al. 2016

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“…A variety of stimuli have been reported to induce formation of NETs, among them are bacteria, fungi, and microbial products (3, 5, 6). Other physiological stimuli include monosodium urate, immune complexes, apoptotic cells, or integrin-mediated signals at high cellular density (7–10). In experimental settings, chemicals with defined mechanisms of action such as phorbol-2-myristate-13-acetate (PMA) or ionomycin also induce NET formation (4).…”

Section: Introductionmentioning

confidence: 99%

Ménage-à-Trois: The Ratio of Bicarbonate to CO2 and the pH Regulate the Capacity of Neutrophils to Form NETs

et al. 2016

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In this study, we identified and characterized the potential of a high ratio of bicarbonate to CO2 and a moderately alkaline pH to render neutrophils prone to undergo neutrophil extracellular trap (NET) formation. Both experimental settings increased the rate of spontaneous NET release and potentiated the NET-inducing capacity of phorbol esters (phorbol-2-myristate-13-acetate), ionomycin, monosodium urate, and LPS. In contrast, an acidic environment impaired NET formation both spontaneous and induced. Our findings indicate that intracellular alkalinization of neutrophils in response to an alkaline environment leads to an increase of intracellular calcium and neutrophil activation. We further found that the anion channel blocker DIDS strongly reduced NET formation induced by bicarbonate. This finding suggests that the effects observed are due to a molecular program that renders neutrophils susceptible to NET formation. Inflammatory foci may be characterized by an acidic environment. Our data indicate that NET formation is favored by the higher pH at the border regions of inflamed areas. Moreover, our findings highlight the necessity for strict pH control during assays of NET formation.

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Instructive influences of phagocytic clearance of dying cells on neutrophil extracellular trap generation

Cited by 36 publications

References 31 publications

Oxidative Burst-Dependent NETosis Is Implicated in the Resolution of Necrosis-Associated Sterile Inflammation

Oxidative Burst-Dependent NETosis Is Implicated in the Resolution of Necrosis-Associated Sterile Inflammation

Cell death, clearance and immunity in the skeletal muscle

Ménage-à-Trois: The Ratio of Bicarbonate to CO2 and the pH Regulate the Capacity of Neutrophils to Form NETs

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