Reprogram inflammation with β-glucan

This 2020 French human cell study found:

“Exposure of mononuclear phagocytes to β-glucan contributes to the induction of innate immune memory, which is associated with long-term epigenetic, metabolic, and functional reprogramming. We investigated how preincubation of human monocytes with particulate β-glucan affects the biological response of macrophages following NLRP3 inflammasome activation.

Upon infection or cellular damage, NLRP3 assembles into a multiprotein inflammasome complex leading to the release of IL-1β. However, NLRP3 inflammasome activity can also be detrimental to the host, and its aberrant chronic activation is associated with severe pathologies.

β-Glucan is a safe molecule present in food products and already widely used in food supplementation. Although β-glucan–induced innate memory is associated with a nonspecific protective effect against infections, the role of this functional reprogramming in autoinflammatory disorders is unknown.

Because of the administration frequency and conservation needs, IL-1β–targeted therapy is invasive, complex, and also costly. In addition, IL-1β, an acute-phase protein, is crucial for effective immune responses to infection, and inhibitors targeting IL-1β may lead to unintended immunosuppressive effects in addition to preventing NLRP3 inflammasome activity in itself.

Targeting the origin of the disease, i.e., NLRP3, would represent the best therapeutic strategy. Most of these candidate drugs directly interact with NLRP3, but none seems to regulate the early activation events upstream of NLRP3 inflammasome assembly.

β-Glucan acted upstream of the NLRP3 inflammasome. β-glucan–induced innate immune memory represses IL-1β–mediated inflammation and support its potential clinical use in NLRP3-driven diseases.”

https://www.jci.org/articles/view/134778 “β-Glucan–induced reprogramming of human macrophages inhibits NLRP3 inflammasome activation in cryopyrinopathies”


This study came closer to addressing causes than others with:

“Targeting the origin of the disease would represent the best therapeutic strategy.”

It’s apparently too recent with a July 27th published date to make it onto https://www.betaglucan.org/i-p/, but earlier β-glucan inflammation studies may be found there.

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