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© Research
Publication : The Journal of clinical investigation

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

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in The Journal of clinical investigation - 27 Jul 2020

Camilli G, Bohm M, Piffer AC, Lavenir R, Williams DL, Neven B, Grateau G, Georgin-Lavialle S, Quintin J,

Link to Pubmed [PMID] – 32716363

Link to DOI [DOI] – 10.1172/JCI134778134778

J. Clin. Invest. 2020 Jul; ():

Exposure of mononuclear phagocytes to β-glucan, a naturally occurring polysaccharide, contributes to the induction of innate immune memory, which is associated with long-term epigenetic, metabolic, and functional reprogramming. Although previous studies have shown that innate immune memory induced by β-glucan confers protection against secondary infections, its impact on autoinflammatory diseases, associated with inflammasome activation and IL-1β secretion, remains poorly understood. In particular, whether β-glucan-induced long-term reprogramming affects inflammasome activation in human macrophages in the context of these diseases has not been explored. We found that NLRP3 inflammasome-mediated caspase-1 activation and subsequent IL-1β production were reduced in β-glucan-reprogrammed macrophages. β-Glucan acted upstream of the NLRP3 inflammasome by preventing potassium (K+) efflux, mitochondrial ROS (mtROS) generation, and, ultimately, apoptosis-associated speck-like protein containing a CARD (ASC) oligomerization and speck formation. Importantly, β-glucan-induced memory in macrophages resulted in a remarkable attenuation of IL-1β secretion and caspase-1 activation in patients with an NLRP3-associated autoinflammatory disease, cryopyrin-associated periodic syndromes (CAPS). Our findings demonstrate that β-glucan-induced innate immune memory represses IL-1β-mediated inflammation and support its potential clinical use in NLRP3-driven diseases.

https://pubmed.ncbi.nlm.nih.gov/32716363