Cathepsin B Is Required for NLRP3 Inflammasome Activation in Macrophages, Through NLRP3 Interaction

Chevriaux, Angélique; Pilot, Thomas; Dérangère, Valentin; Simonin, Harmonie; Martine, Pierre; Chalmin, Fanny; Ghiringhelli, François; Rébé, Cédric

doi:10.3389/fcell.2020.00167

Cited by 114 publications

(91 citation statements)

References 41 publications

(60 reference statements)

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“…We found that challenge of TG induced release of cathepsin B from the lysosome to the cytoplasm, which subsequently activates extrinsic apoptotic pathways. Moreover, we showed cathepsin B is a prerequisite for caspase-1 activation, which is the same observance with the very recent report [12]. Our results show that TG-induced macrophage cell death is mediated by the cytosolic release of cathepsin B from the lysosome.…”

Section: Introductionsupporting

confidence: 93%

Cathepsin B Is Implicated in Triglyceride (TG)-Induced Cell Death of Macrophage

Jung

Kim

et al. 2020

Korean J Clin Lab Sci.

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Macrophage cell death contributes to the formation of plaque, leading to the development of atherosclerosis. The accumulation of triglyceride (TG) is also associated with the pathogenesis of atherosclerosis. A previous study reported that TG induces the cell death of macrophages. This study examined whether the cytoplasmic release of cathepsin B from lysosome is associated with the TG-induced cell death of macrophage. The release of cathepsin B was increased in the TG-treated THP-1 macrophages, but the TG treatment did not affect cathepsin B expression. Furthermore, the inhibition of cathepsin B by its inhibitor, CA-074 Me, partially inhibited the TG-induced cell death of macrophage. TG-triggered macrophage cell death is mediated by the activation of caspase-1,-2, and apoptotic caspases. Therefore, this study investigated whether cathepsin B is implicated in the activation of these caspases. The inhibition of cathepsin B blocked the activation of caspase-7,-8, and-1 but did not affect the activity of caspase-3,-9, and-2. Overall, these results suggest that TG-induced cytoplasmic cathepsin B causes THP-1 macrophage cell death by activating caspase-1, leading to subsequent activation of the extrinsic apoptotic pathway.

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Section: Introductionsupporting

confidence: 93%

Cathepsin B Is Implicated in Triglyceride (TG)-Induced Cell Death of Macrophage

Jung

Kim

et al. 2020

Korean J Clin Lab Sci.

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“…The third pathway involves an increase in reactive oxygen species (ROS) synthesis. All these steps will converge to NLRP3 activation, recruitment of ASC (apoptosis associated speck-like protein containing a CARD domain) and pro-caspase-1, and IL-1β and IL-18 maturation [ 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

Interleukin-1β and Cancer

Rébé

Ghiringhelli

2020

Cancers

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166

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Within a tumor, IL-1β is produced and secreted by various cell types, such as immune cells, fibroblasts, or cancer cells. The IL1B gene is induced after “priming” of the cells and a second signal is required to allow IL-1β maturation by inflammasome-activated caspase-1. IL-1β is then released and leads to transcription of target genes through its ligation with IL-1R1 on target cells. IL-1β expression and maturation are guided by gene polymorphisms and by the cellular context. In cancer, IL-1β has pleiotropic effects on immune cells, angiogenesis, cancer cell proliferation, migration, and metastasis. Moreover, anti-cancer treatments are able to promote IL-1β production by cancer or immune cells, with opposite effects on cancer progression. This raises the question of whether or not to use IL-1β inhibitors in cancer treatment.

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“…The main components responsible for this maturation are multiprotein complexes, named inflammasomes. In response to several types of stimulation, they enable the activation of caspase-1, which, in turn, cleaves pro-IL-1β into IL-1β (Chevriaux et al, 2020). Inflammasomes may also be activated by viruses (Hayward, Mathur, Ngo, & Man, 2018).…”

Section: Effects On Protease-mediated Cytokine Productionmentioning

confidence: 99%

Can the hyperthermia‐mediated heat shock factor/heat shock protein 70 pathway dampen the cytokine storm during SARS‐CoV‐2 infection?

Rébé

Ghiringhelli

Garrido

2021

British J Pharmacology

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a major global public health problem. Infection by this virus involves many pathophysiological processes, such as a "cytokine storm," that is, very aggressive inflammatory response that offers new perspectives for the management and treatment of patients. Here, we analyse relevant mechanism involved in the hyperthermia-mediated heat shock factors (HSFs)/heat shock proteins (HSP)70 pathway which may provide a possible treatment tool.

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Cathepsin B Is Required for NLRP3 Inflammasome Activation in Macrophages, Through NLRP3 Interaction

Cited by 114 publications

References 41 publications

Cathepsin B Is Implicated in Triglyceride (TG)-Induced Cell Death of Macrophage

Cathepsin B Is Implicated in Triglyceride (TG)-Induced Cell Death of Macrophage

Interleukin-1β and Cancer

Can the hyperthermia‐mediated heat shock factor/heat shock protein 70 pathway dampen the cytokine storm during SARS‐CoV‐2 infection?

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