IntroductionNeuroinflammation, which is driven by microglial activation, contributes to neurodegeneration. The myokine irisin exerts anti-inflammatory effects, potentially through microRNA-mediated regulation of inflammasome components.
However, the underlying molecular mechanisms remain incompletely defined. In this in vitro study we investigated whether irisin attenuates the β-amyloid (Aβ)-induced activation of human microglia via miR-451a-, miR-223-3p-, and miR-7-5p-dependent modulation of NLRP3-related genes.MethodsFor this aim, human immortalized microglia (hTERT) were LPS primed and Aβ1-42, stimulated in the presence or absence of irisin.
The expression of NLRP3, TLR4, caspase-1, IL-1β, IL-18, PYCARD, and selected microRNAs (miR-451a, miR-223-3p, and miR-7-5p) was quantified by digital droplet PCR. TLR4 expression in hTERT cells was analyzed by flow cytometry and intracellular ASC speck formation with NLRP3 colocalization and NF-κB nuclear translocation was measured by imaging flow cytometry.
Cytokine release was measured in the supernatants using ELISA.
Frontiers in Immunology published a clinical update in Infectious Disease on 23 Apr 2026.
The item focuses on Irisin hampers β-amyloid-induced microglial inflammation via the miR-451a/TLR4/NLRP3 axis.
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