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Updated: Jan 15, 2026
Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
METTL3-mediated N6-methyladenosine modification regulates NLRP3 inflammasome activation in chronic suppurative otitis
1Department of Otolaryngology, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui, China; Department of Otolaryngology, Fuyang Hospital Of Anhui Medical University, Fuyang 236113, Anhui, China; Department of Otolaryngology, Peking University Shenzhen Hospital, Shenzhen 518036, China.
Background:
Chronic suppurative otitis media (CSOM) is a common inflammatory condition characterized by persistent ear discharge and hearing loss. Recent studies have highlighted the importance of the NLRP3 inflammasome in the pathogenesis of various inflammatory diseases, including CSOM. Here, we investigated the role of METTL3 and N6-methyladenosine (m6A) modification in the regulation of NLRP3 inflammasome activation in CSOM.
Methods:
CSOM model mice were established by intraperitoneally injected with lipopolysaccharide (LPS) and middle ear tissues were collected for analysis. Inflammatory cytokines including TNF-α, IL-1β, IFN-γ, and IL-6 were evaluated, as well as the levels of m6A related genes. The potential regulatory effects of METTL3 mediated m6A modification of NLRP3 was further studied to explain the inflammatory response in CSOM.
Results:
We found that METTL3 overexpression increased the m6A level and mRNA stability of NLRP3, leading to enhanced inflammasome activation and production of inflammatory cytokines. Conversely, silencing METTL3 reduced NLRP3 expression and inflammasome activity. Rescue experiments with NLRP3 overexpression confirmed that the effects of METTL3 on inflammation were mediated through NLRP3. Additionally, the NLRP3 inhibitor MCC950 reversed the pro-inflammatory effects of METTL3 overexpression.
Conclusions:
Our findings suggest that METTL3-mediated m6A modification plays a critical role in NLRP3 inflammasome activation and the inflammatory response in CSOM. Targeting the METTL3/NLRP3 axis may provide a novel therapeutic strategy for the treatment of CSOM.
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