β-Glucan–induced reprogramming of human macrophages inhibits NLRP3 inflammasome activation in cryopyrinopathies

Camilli, Giorgio; Bohm, Mathieu; Piffer, Alícia Corbellini; Lavenir, Rachel; Williams, David L.; Neven, Bénédicte; Grateau, Gilles; Georgin-Lavialle, S.; Quintin, Jessica

doi:10.1172/jci134778

Cited by 57 publications

(60 citation statements)

References 79 publications

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“…β-Glucan-induced immune reprogramming, which is critical for innate immune memory, suppresses ASC oligomerization and speck formation activation in human macrophages to attenuate the NLRP3 inflammasome formation via inhibition of K + efflux and generation of mtROS. 188 β-glucan-induced memory was beneficial for attenuating IL-1β secretion in macrophages from patients with the NLRP3-associated autoinflammatory disease cryopyrin-associated periodic syndrome (CAPS), suggesting that attenuating IL-1β secretion may have therapeutic potential for NLRP3-related diseases. 188 It will also be important to determine how innate immune memory affects NLRP3 inflammasome assembly and inhibits activating signals.…”

Section: Introductionmentioning

confidence: 99%

An update on the regulatory mechanisms of NLRP3 inflammasome activation

et al. 2021

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The NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome is a multiprotein complex involved in the release of mature interleukin-1β and triggering of pyroptosis, which is of paramount importance in a variety of physiological and pathological conditions. Over the past decade, considerable advances have been made in elucidating the molecular mechanisms underlying the priming/licensing (Signal 1) and assembly (Signal 2) involved in NLRP3 inflammasome activation. Recently, a number of studies have indicated that the priming/licensing step is regulated by complicated mechanisms at both the transcriptional and posttranslational levels. In this review, we discuss the current understanding of the mechanistic details of NLRP3 inflammasome activation with a particular emphasis on protein-protein interactions, posttranslational modifications, and spatiotemporal regulation of the NLRP3 inflammasome machinery. We also present a detailed summary of multiple positive and/or negative regulatory pathways providing upstream signals that culminate in NLRP3 inflammasome complex assembly. A better understanding of the molecular mechanisms underlying NLRP3 inflammasome activation will provide opportunities for the development of methods for the prevention and treatment of NLRP3 inflammasome-related diseases.

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Section: Introductionmentioning

confidence: 99%

An update on the regulatory mechanisms of NLRP3 inflammasome activation

et al. 2021

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“…For example, GAG-mediated inflammasome activation is protective in a murine colitis model [ 55 ]. Additionally, β-(1,3)-glucan mediates reprogramming and training of innate immune cells [ 70 ], and β-(1,3)-glucan–reprogrammed macrophages have impaired canonical NLRP3 inflammasome activation [ 71 ]. When macrophages from patients with cryopyrin-associated autoinflammatory syndrome are treated with β-(1,3)-glucan, they have reduced caspase-1 activation and IL-1β release compared with untreated macrophages [ 71 ], which could be therapeutically beneficial for these patients.…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, β-(1,3)-glucan mediates reprogramming and training of innate immune cells [ 70 ], and β-(1,3)-glucan–reprogrammed macrophages have impaired canonical NLRP3 inflammasome activation [ 71 ]. When macrophages from patients with cryopyrin-associated autoinflammatory syndrome are treated with β-(1,3)-glucan, they have reduced caspase-1 activation and IL-1β release compared with untreated macrophages [ 71 ], which could be therapeutically beneficial for these patients. These finding should open new perspectives in studies focused on the ability of fungal polysaccharides to modulate inflammasome activation as potential therapeutic strategies.…”

Section: Discussionmentioning

confidence: 99%

Role of inflammasomes/pyroptosis and PANoptosis during fungal infection

2021

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“…The mechanisms via which curdlan reduces innate immune response remain unclear. Possibly, part of the ingested β-glucan enters the system and induces innate immune memory [ 68 , 69 , 70 ]. However, curdlan-mediated innate immune memory generally leads to innate immune training, which increases the response to a second immune challenge, such as LPS [ 69 , 71 ].…”

Section: Discussionmentioning

confidence: 99%

Dietary Curdlan Enhances Bifidobacteria and Reduces Intestinal Inflammation in Mice

et al. 2021

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β-glucan consumption is known for its beneficial health effects, but the mode of action is unclear. While humans and mice lack the required enzymes to digest β-glucans, certain intestinal microbes can digest β-glucans, triggering gut microbial changes. Curdlan, a particulate β-glucan isolated from Alcaligenes faecalis, is used as a food additive. In this study we determined the effect of curdlan intake in mice on the intestinal microbiota and dextran sodium sulfate (DSS)-induced intestinal inflammation. The effect of curdlan on the human intestinal microbiota was assessed using i-screen, an assay for studying anaerobic microbial interactions. Mice received oral gavage with vehicle or curdlan for 14 days followed by DSS for 7 days. The curdlan-fed group showed reduced weight loss and colonic inflammation compared to the vehicle-fed group. Curdlan intake did not induce general microbiota community changes, although a specific Bifidobacterium, closely related to Bifidobacterium choerinum, was observed to be 10- to 100-fold more prevalent in the curdlan-fed group under control and colitis conditions, respectively. When tested in i-screen, curdlan induced a global change in the microbial composition of the healthy intestinal microbiota from a human. Overall, these results suggest that dietary curdlan induces microbiota changes that could reduce intestinal inflammation.

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β-Glucan–induced reprogramming of human macrophages inhibits NLRP3 inflammasome activation in cryopyrinopathies

Cited by 57 publications

References 79 publications

An update on the regulatory mechanisms of NLRP3 inflammasome activation

An update on the regulatory mechanisms of NLRP3 inflammasome activation

Role of inflammasomes/pyroptosis and PANoptosis during fungal infection

Dietary Curdlan Enhances Bifidobacteria and Reduces Intestinal Inflammation in Mice

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