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Modulating NLRP3 splicing with antisense oligonucleotides to control pathological inflammation.

Roni Klein1,2, Janset Onyuru3, Jessica L Centa1,4

  • 1Center for Genetic Diseases, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064, United States.

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|November 8, 2025
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Scientists used splice-switching antisense oligonucleotides (ASOs) to control the NLRP3 inflammasome, a key player in inflammation. This approach reduces harmful inflammation by targeting specific NLRP3 protein forms, offering a potential new therapy.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Inflammation is crucial for healing but pathogenic when unresolved.
  • The NLR family pyrin domain-containing 3 (NLRP3) inflammasome is a key regulator of innate immunity and a therapeutic target for inflammatory diseases.
  • Alternative splicing of NLRP3 RNA influences inflammasome activation, with some isoforms exhibiting reduced function.

Purpose of the Study:

  • To investigate the use of splice-switching antisense oligonucleotides (ASOs) to modulate NLRP3 inflammasome activity.
  • To identify ASOs that induce non-inflammatory NLRP3 isoforms.
  • To evaluate the therapeutic potential of ASO-mediated NLRP3 modulation in preclinical models.

Main Methods:

  • Screening of antisense oligonucleotides (ASOs) targeting different exons of NLRP3 RNA.
  • Assessment of ASO efficacy in modulating NLRP3 splicing and protein levels in vitro.
  • Evaluation of inflammasome signaling in response to ASO treatment.
  • Testing the most effective ASO in mouse models of acute inflammation and cryopyrin-associated periodic syndrome.

Main Results:

  • Several ASOs were identified that effectively modulate NLRP3 splicing, reduce NLRP3 protein expression, and decrease inflammasome signaling in vitro.
  • The lead ASO candidate demonstrated significant suppression of systemic inflammation in vivo.
  • The ASO successfully reduced inflammation in mouse models of acute inflammation and cryopyrin-associated periodic syndrome.

Conclusions:

  • ASOs can be utilized to engineer proteins with modified functions by targeting alternative splicing.
  • This study demonstrates the potential of ASO-based therapeutics for treating pathological inflammation by reducing functional NLRP3.
  • Targeting NLRP3 splicing with ASOs represents a promising strategy for managing inflammatory diseases.