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Trained immunity, driven by β-glucan, worsens inflammatory arthritis by reprogramming macrophages. Targeting trained immunity with iFSP1 and Remodelin offers a novel therapeutic strategy for arthritis.

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Area of Science:

  • Immunology
  • Inflammation Biology
  • Arthritis Research

Background:

  • Trained immunity, a form of innate immune memory, can lead to hyperinflammation.
  • Inflammatory arthritis shares characteristics with trained immunity, with potential environmental triggers like β-glucan.
  • The role of trained immunity in inflammatory arthritis progression is not well understood.

Purpose of the Study:

  • To investigate the contribution of trained immunity to inflammatory arthritis.
  • To explore the mechanisms by which trained immunity affects arthritis pathogenesis.
  • To evaluate therapeutic strategies targeting trained immunity in arthritis.

Main Methods:

  • Induction of experimental trained immunity using β-glucan in a collagen-induced arthritis (CIA) rat model.
  • Adoptive transfer of trained macrophages to assess their impact on arthritis symptoms.
  • Analysis of molecular pathways, including lipid peroxidation, ferroptosis, and ac4C modification, in fibroblast-like synoviocytes (FLS).
  • Evaluation of a combination therapy involving iFSP1 and Remodelin.

Main Results:

  • β-glucan-induced trained immunity exacerbated inflammation and arthritis severity in the CIA model.
  • Adoptively transferred trained macrophages intensified arthritis symptoms.
  • Trained macrophages suppressed FLS ferroptosis via IL-1β/NAT10/FSP1 mRNA ac4C modification.
  • Combined iFSP1 and Remodelin treatment reduced arthritis severity and restored ferroptosis sensitivity.
  • A feedback loop between CIA induction and β-glucan training accelerated disease progression.

Conclusions:

  • Trained immunity, induced by β-glucan, is a significant factor in inflammatory arthritis pathogenesis.
  • Trained macrophages modulate FLS ferroptosis through specific molecular pathways.
  • Targeting trained immunity presents a promising therapeutic avenue for inflammatory arthritis.