Pyroptosis versus necroptosis: similarities, differences, and crosstalk

Frank, Daniel; Vince, James E.

doi:10.1038/s41418-018-0212-6

Cited by 793 publications

(623 citation statements)

References 205 publications

(268 reference statements)

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“…Lytic cell death requires gasdermin D (GSDMD) for pyroptosis and mixed lineage kinase domain like pseudokinase (MLKL) for necroptosis. Both GSDMD and MLKL result in IL-1β-driven inflammation, which is from caspase-1 activation [35]. Pyroptotic and necroptotic cell death show distinct morphological differences; reduced cell swelling and flattened cytoplasm in pyroptosis, and cell swelling and subsequent osmolysis in necroptosis.…”

Section: Discussionmentioning

confidence: 99%

Sea Hare Hydrolysate-Induced Reduction of Human Non-Small Cell Lung Cancer Cell Growth through Regulation of Macrophage Polarization and Non-Apoptotic Regulated Cell Death Pathways

Nyiramana

Cho

Kim

et al. 2020

Cancers

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Sea hare-derived compounds induce macrophage activation and reduce asthmatic parameters in mouse models of allergic asthma. These findings led us to study the role of sea hare hydrolysates (SHH) in cancer pathophysiology. SHH treatment-induced M1 macrophage activation in RAW264.7 cells, peritoneal macrophages, and THP-1 cells, as did lipopolysaccharide (LPS) (+ INF-γ), whereas SHH reduced interleukin (IL)-4 (+IL-13)-induced M2 macrophage polarization. In addition, SHH treatment inhibited the actions of M1 and M2 macrophages, which have anticancer and pro-cancer effects, respectively, in non-small cell lung cancer cells (A549 and HCC-366) and tumor-associated macrophages (TAMs). Furthermore, SHH induced G2/M phase arrest and cell death in A549 cells. SHH also downregulated STAT3 activation in macrophages and A549 cells, and the down-regulation was recovered by colivelin, a STAT3 activator. SHH-induced reduction of M2 polarization and tumor growth was blocked by colivelin treatment. SHH-induced cell death did not occur in the manner of apoptotic signaling pathways, while the death pattern was mediated through pyroptosis/necroptosis, which causes membrane rupture, formation of vacuoles and bleb, activation of caspase-1, and secretion of IL-1β in SHH-treated A549 cells. However, a combination of SHH and colivelin blocked caspase-1 activation. Z-YVAD-FMK and necrostatin-1, pyrotosis and necroptosis inhibitors, attenuated SHH's effect on the cell viability of A549 cells. Taken together, SHH showed Cancers 2020, 12, 726 2 of 24 anticancer effects through a cytotoxic effect on A549 cells and a regulatory effect on macrophages in A549 cells. In addition, the SHH-induced anticancer effects were mediated by non-apoptotic regulated cell death pathways under STAT3 inhibition. These results suggest that SHH may be offered as a potential remedy for cancer immunotherapy.

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Section: Discussionmentioning

confidence: 99%

Sea Hare Hydrolysate-Induced Reduction of Human Non-Small Cell Lung Cancer Cell Growth through Regulation of Macrophage Polarization and Non-Apoptotic Regulated Cell Death Pathways

Nyiramana

Cho

Kim

et al. 2020

Cancers

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“…The term 'Necroptosis' refers to a non-apoptotic cell death pathway and was coined by a study that focused on the role of a drug named necrostatin-1 (nec-1), which blocks the genetic determinant receptor-interacting serine/threonine-protein kinase 1 (RIPK1). Necroptosis induces inflammation, thereby slowing down the recovery process, and RIPK1 is responsible for inducing necroptosis in the cells treated with TNF-α [22]. Recent insights into the therapeutic efficacy of nec-1 Cells 2020, 9, 750 5 of 20 after ICH include its ability to inhibit TNF-α -induced necroptosis to limit cell death and a reduction in hematoma volume in mice [23,24].…”

Section: Necrosis Apoptosis and Necroptosismentioning

confidence: 99%

“…The most common inflammasome sensors are absent in melanoma 2 (AIM2), and pyrin and nucleotide-binding oligomerization domain-like receptors (NLRs). The most prevalently studied inflammasome is NLR pyrin domain containing 3 (NLRP3) and it is thought to mediate various neurodegenerative and neurological disorders [22,27]. Pyroptosis involves the release of proinflammatory cytokines, especially IL-1β/IL-18; this, when combined with caspase-1 and inflammasome activity, causes the cells to swell and burst, thus leading to cell death.…”

Section: Pyroptosismentioning

confidence: 99%

A Role for Endoplasmic Reticulum Stress in Intracerebral Hemorrhage

Thangameeran

Tsai

Hung

et al. 2020

Cells

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The endoplasmic reticulum (ER) is an intracellular organelle that performs multiple functions, such as lipid biosynthesis, protein folding, and maintaining intracellular calcium homeostasis. Thus, conditions wherein the ER is unable to fold proteins is defined as ER stress, and an inbuilt quality control mechanism, called the unfolded protein response (UPR), is activated during ER stress, which serves as a recovery system that inhibits protein synthesis. Further, based on the severity of ER stress, the response could involve both proapoptotic and antiapoptotic phases. Intracerebral hemorrhage (ICH) is the second most common subtype of cerebral stroke and many lines of evidence have suggested a role for the ER in major neurological disorders. The injury mechanism during ICH includes hematoma formation, which in turn leads to inflammation, elevated intracranial pressure, and edema. a proper understanding of the injury mechanism(s) is required to effectively treat ICH and closing the gap between our current understanding of ER stress mechanisms and ICH injury can lead to valuable advances in the clinical management of ICH.Cells 2020, 9, 750 2 of 20 because of cardiovascular conditions, with hypertension playing a major role. PBI is characterized by mechanical injury followed by a mass effect with the initial ictus causing physical tissue disruption that then leads to pathophysiological conditions in the brain.A sudden rise in intracranial hematoma volume causes an increase in barotrauma and reduces blood flow to the area of the ictus [4,5]. Typically, PBI is followed by SBI, which is considered as a devastating stage after ICH, and the severity of SBI depends on the rate of recovery and location of the ICH. SBI involves the neuroinflammatory response to the triggering of the coagulation cascade through activation of the immune system. The inflammation size is based on the volume and position of the hematoma [5][6][7]. The various pathological factors responsible for SBI include the host immune response, release of thrombin, release of clot components (iron and heme)

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“…This interaction leads to a number of molecular and cellular signals that serve to protect the host on cellular and organism levels. One such innate signaling system is the formation of inflammasomes which are intracellular multi-protein complexes that regulate an inflammatory type of cell death called pyroptosis, as well as, the production of mature forms of the inflammatory cytokines IL-1β and IL-18 [2]. Macrophages and myeloid dendritic cells (mDCs) are the primary producers of these potent pro-inflammatory cytokines, which drive type 1 immunity in natural killer cells and T-cells [3].…”

Section: Introductionmentioning

confidence: 99%

“…Recognition of an appropriate PAMP or DAMP by one of these adapter proteins leads to apoptosis-associated speck-like molecule containing a caspase recruitment domain (ASC) assembly and oligomerization followed by pro-caspase-1 recruitment to the complex. Pro-caspase-1 autocatalyzation to active caspase-1 allows for cleavage of pro-IL-1β and pro-IL-18 to their active forms, IL-1β and IL-18, and then secretion into the extracellular space (reviewed in [2,9,10]). There are multiple sensors and caspases that can lead to inflammasome cytokine release, but the caspase-1 pathway is thought to be the most relevant in viral infection [11,12].…”

Section: Introductionmentioning

confidence: 99%

Herpes Simplex Virus type 1 Inflammasome Activation in Human Macrophages is Dependent on NLRP3, ASC, and Caspase-1

Karaba

Figueroa

Massaccesi

et al. 2019

Preprint

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20 Review and Editing 21 22 23 Abstract:24 The pro-inflammatory cytokines interleukin (IL)-1 and IL-18 are products of activation of the 25 inflammasome, an innate sensing system, and important in the pathogenesis of herpes simplex 26 type 1 (HSV-1). The release of IL-18 and IL-1 from monocytes/macrophages is critical for 27 protection from HSV-1 based on animal models of encephalitis and genital infection, yet if and 28 how HSV-1 activates inflammasomes in human macrophages is unknown. To investigate this, 29 we utilized both primary human monocyte derived macrophages and human monocytic cell 30 lines (THP-1 cells) with various inflammasome components knocked-out. We found that HSV-1 31 activates inflammasome signaling in pro-inflammatory primary human macrophages.32 Additionally, HSV-1 inflammasome activation is dependent on nucleotide-binding domain and 33 leucine-rich repeat-containing receptor 3 (NLRP3), apoptosis-associated speck-like molecule 34 containing a caspase recruitment domain (ASC), and caspase-1, but not on absent in melanoma 35 2 (AIM2), or gamma interferon-inducible protein 16 (IFI16). Ultraviolet irradiation of HSV-1 36 enhanced inflammasome activation, demonstrating that viral replication suppresses 37 inflammasome activation. These results confirm that HSV-1 is capable of activating the 38 inflammasome in human macrophages through an NLRP3 dependent process and that the virus 39 has an NLRP3 specific mechanism to inhibit inflammasome activation in monocytes and 40 macrophages. 41 42 43 44 3 45 Author Summary: 46The inflammasome is a multi-protein complex that forms in response to pathogens and 47 cellular damage. Active inflammasomes recruit pro-caspase-1 via ASC and cleave the cytokine 48 precursors pro-IL-1 and pro-IL-18 into mature IL-1 and IL-18. These cytokines serve to 49 activate other immune cells that either repair the damage or attempt to clear the invading 50 pathogen. Upon activation, the inflammasome also promotes an inflammatory form of cell 51 death called pyroptosis. Herpes simplex virus type 1 (HSV-1) is a common human pathogen that 52 can cause cold sores, genital ulcers, encephalitis, and blindness. HSV-1 infection leads to 53 induction of IL-1 and IL-18, but whether it is capable of activating inflammasomes in 54 macrophages, which play a role in severe forms of HSV-1 infection, was unclear. Here, we 55 infected both primary human macrophages and a macrophage/monocytic cell line, THP-1 cells, 56 with HSV-1. We found that HSV-1 does activate inflammasome signaling in macrophages in a 57 process dependent on NLRP3, ASC, and caspase-1. This is important because it illustrates the 58 mechanism by which HSV-1 infection leads to inflammasome activation in macrophages, known 59 to be crucial for protection from severe disease in mouse models. 60 61 62 63 64 65 66 4 67 Introduction: 68 The ability to quickly recognize and respond to pathogens is essential to host survival. 69 The first opportunity to do so lies in the innate immune response. One of the most essential 70 aspe...

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Pyroptosis versus necroptosis: similarities, differences, and crosstalk

Abstract: How critical are GSDMD membrane pores for IL-1β release and inflammatory responses in different diseases?

Cited by 793 publications

References 205 publications

Sea Hare Hydrolysate-Induced Reduction of Human Non-Small Cell Lung Cancer Cell Growth through Regulation of Macrophage Polarization and Non-Apoptotic Regulated Cell Death Pathways

Sea Hare Hydrolysate-Induced Reduction of Human Non-Small Cell Lung Cancer Cell Growth through Regulation of Macrophage Polarization and Non-Apoptotic Regulated Cell Death Pathways

A Role for Endoplasmic Reticulum Stress in Intracerebral Hemorrhage

Herpes Simplex Virus type 1 Inflammasome Activation in Human Macrophages is Dependent on NLRP3, ASC, and Caspase-1

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