Specific NLRP3 Inflammasome Assembling and Regulation in Neutrophils: Relevance in Inflammatory and Infectious Diseases

Paget, Christophe; Doz-Deblauwe, Émilie; Winter, Nathalie; Briard, Benoit

doi:10.3390/cells11071188

Cited by 30 publications

(22 citation statements)

References 145 publications

(233 reference statements)

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“…Subsequent studies have verified that neutrophils can assemble functional inflammasome platforms initiated by AIM2, 75 NLRC4, 35,75–79 NLRP1, 75 NLRP3, 32,34,51,57,75,80,81 and pyrin/MEFV 75,78 . These are discussed in detail below regarding the differential induction of IL‐1β release versus pyroptosis as downstream responses to inflammasome activation in neutrophils.…”

Section: Inflammasomes and Gasdermins As Critical Regulators Of Pyrop...mentioning

confidence: 91%

Pyroptosis in neutrophils: Multimodal integration of inflammasome and regulated cell death signaling pathways

Dubyak

Miller

Pearlman

2023

Immunological Reviews

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Pyroptosis is a proinflammatory mode of lytic cell death mediated by accumulation of plasma membrane (PM) macropores composed of gasdermin-family (GSDM) proteins.It facilitates two major functions in innate immunity: (i) elimination of intracellular replicative niches for pathogenic bacteria; and (ii) non-classical secretion of IL-1 family cytokines that amplify host-beneficial inflammatory responses to microbial infection or tissue damage. Physiological roles for gasdermin D (GSDMD) in pyroptosis and IL-1β release during inflammasome signaling have been extensively characterized in macrophages. This involves cleavage of GSDMD by caspase-1 to generate GSDMD macropores that mediate IL-1β efflux and progression to pyroptotic lysis. Neutrophils, which rapidly accumulate in large numbers at sites of tissue infection or damage, become the predominant local source of IL-1β in coordination with their potent microbiocidal capacity. Similar to macrophages, neutrophils express GSDMD and utilize the same spectrum of diverse inflammasome platforms for caspase-1-mediated cleavage of GSDMD. Distinct from macrophages, neutrophils possess a remarkable capacity to resist progression to GSDMD-dependent pyroptotic lysis to preserve their viability for efficient microbial killing while maintaining GSDMD-dependent mechanisms for export of bioactive IL-1β. Rather, neutrophils employ cell-specific mechanisms to conditionally engage GSDMD-mediated pyroptosis in response to bacterial pathogens that use neutrophils as replicative niches. GSDMD and pyroptosis have also been mechanistically linked to induction of NETosis, a signature neutrophil pathway that expels decondensed nuclear DNA into extracellular compartments for immobilization and killing of microbial pathogens. This review summarizes a rapidly growing number of recent studies that have produced new insights, unexpected mechanistic nuances, and some controversies regarding the regulation of, and roles for, neutrophil inflammasomes, pyroptosis, and GSDMs in diverse innate immune responses.

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Section: Inflammasomes and Gasdermins As Critical Regulators Of Pyrop...mentioning

confidence: 91%

Pyroptosis in neutrophils: Multimodal integration of inflammasome and regulated cell death signaling pathways

Dubyak

Miller

Pearlman

2023

Immunological Reviews

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“…In addition, NETosis allows neutrophils to abundantly release of S100A8/A9 proteins and induce the recruitment of more neutrophils ( 59 ). NETs can activate macrophage NLRP3 to produce IL-1β and IL-18, thus exerting powerful proinflammatory effects, where IL-18 in turn can promote an increase in circulating NETs, creating a vicious cycle that further amplifies inflammation ( 60 , 61 ). Here, notably, patients with common LNK loss-of-function activate oxidized phospholipid (OxPL)-dependent platelet-neutrophil aggregation in vivo , promoting NETosis ( 62 ), and it has been demonstrated that inactivation of OxPL by antibodies after MI in mice protects cardiomyocyte viability and reduces infarct size ( 63 ).…”

Section: Powerful Modulation Of Ventricular Remodeling By Immune Cellsmentioning

confidence: 99%

Immune cells drive new immunomodulatory therapies for myocardial infarction: From basic to clinical translation

Nian

Huang

2023

Front. Immunol.

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The high incidence of heart failure secondary to myocardial infarction (MI) has been difficult to effectively address. MI causes strong aseptic inflammation, and infiltration of different immune cells and changes in the local inflammatory microenvironment play a key regulatory role in ventricular remodeling. Therefore, the possibility of improving the prognosis of MI through targeted immunity has been of interest and importance in MI. However, previously developed immune-targeted therapies have not achieved significant success in clinical trials. Here, we propose that the search for therapeutic targets from different immune cells may be more precise and lead to better clinical translation. Specifically, this review summarizes the role and potential therapeutic targets of various immune cells in ventricular remodeling after MI, especially monocytes/macrophages and neutrophils, as a way to demonstrate the importance and potential of immunomodulatory therapies for MI. In addition, we analyze the reasons for the failure of previous immunomodulatory therapies and the issues that need to be addressed, as well as the prospects and targeting strategies of using immune cells to drive novel immunomodulatory therapies, hoping to advance the development of immunomodulatory therapies by providing evidence and new ideas.

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“…IL-1 can induce the expression of proinflammatory cytokines or chemokines such as IL-6, IL-8, and CCL2 in inflammatory sites. The changes in the expression of these inflammatory cytokines or chemokines recruit monocytes and neutrophils to migrate to infection, injury, and necrosis sites to engulf pathogens, inducing local inflammatory response, and even promoting the activation of dendritic cells and neutrophils; this series of chain reactions triggered by IL-1 will eventually help the host to resist the invasion of pathogens and maintain the homeostasis in the host’s intestine [ 40 , 41 , 42 ]. In addition, Judy Lieberman’s research shows that NLRP3 can affect lamina propria mononuclear cells to secrete more IL-1β.…”

Section: The Relationship Between the Nlrp3 Inflammasome And Intestin...mentioning

confidence: 99%

NLRP3 and Gut Microbiota Homeostasis: Progress in Research

Pan

Jian

Wang³

et al. 2022

Cells

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The inflammasome is a platform for inflammatory signaling, and the NLRP3 inflammasome recognizes stimuli in vitro and in vivo, and releases inflammatory cytokines that trigger inflammation and pyroptosis. In the gut, the NLRP3 inflammasome is a key sensor for protecting the body from damage and exogenous pathogens. It plays a fundamental role in maintaining the stability of the gut’s immune system. We focus on the role of NLRP3 as a key node in maintaining the homeostasis of gut microbiota which has not been fully highlighted in the past; gut microbiota and innate immunity, as well as the NLRP3 inflammasome, are discussed in this article.

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Specific NLRP3 Inflammasome Assembling and Regulation in Neutrophils: Relevance in Inflammatory and Infectious Diseases

Cited by 30 publications

References 145 publications

Pyroptosis in neutrophils: Multimodal integration of inflammasome and regulated cell death signaling pathways

Pyroptosis in neutrophils: Multimodal integration of inflammasome and regulated cell death signaling pathways

Immune cells drive new immunomodulatory therapies for myocardial infarction: From basic to clinical translation

NLRP3 and Gut Microbiota Homeostasis: Progress in Research

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