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Impaired microRNA processing in neutrophils from rheumatoid arthritis patients confers their pathogenic profile.

Ivan Arias De la Rosa1, Carlos Perez-Sanchez2, Patricia Ruiz-Limon3

  • 1Rheumatology service, Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC)/Reina Sofia Hospital/University of Cordoba, Cordoba, Spain.

Haematologica
|October 15, 2020
PubMed

Insights

Rheumatoid arthritis neutrophils show low microRNA levels, contributing to inflammation. Autoantibodies and inflammatory markers worsen this, but therapies like infliximab can restore miRNA balance and reduce neutrophil inflammation.

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Rheumatoid arthritis (RA) is characterized by chronic inflammation and autoimmunity.
  • Neutrophils play a critical role in RA pathogenesis.
  • MicroRNAs (miRNAs) are key regulators of gene expression implicated in various diseases.

Purpose of the Study:

  • To investigate miRNA expression patterns in neutrophils from RA patients.
  • To determine the role of autoantibodies and inflammatory components in regulating miRNA in RA neutrophils.
  • To analyze the modulation of miRNA by biological therapies.

Main Methods:

  • Neutrophil isolation from peripheral blood and synovial fluid of RA patients and healthy donors.
  • miRNA array analysis using nCounter technology.
  • In vitro treatments with autoantibodies, cytokines (TNF-α, IL-6), and biological therapies (tocilizumab, infliximab).
  • Gene transfection and knockdown experiments (DICER).

Main Results:

  • RA neutrophils exhibit global miRNA downregulation and impaired biogenesis, correlating with disease activity.
  • Autoantibodies and inflammatory markers (TNF-α) decrease miRNA expression and enhance pro-inflammatory gene targets.
  • Infliximab treatment reversed these effects, normalizing miRNA levels.
  • Specific miRNAs (miR-223, -126, -148a) modulated neutrophil inflammation, survival, and migration.
  • Synovial fluid neutrophils showed further miRNA downregulation.

Conclusions:

  • RA neutrophils have low miRNA abundance, driven by autoantibodies and inflammation, contributing to their pathogenic activation.
  • Impaired miRNA biogenesis in RA neutrophils exacerbates the downregulation of migration and inflammation-related miRNAs.
  • Biological therapies targeting TNF-α and IL-6 receptor can modulate neutrophil miRNA levels and reduce inflammation.

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