SARS-CoV-2 spike protein promotes inflammatory cytokine activation and aggravates rheumatoid arthritis

A Ram Lee1,2,3, Jin Seok Woo1,2, Seon-Yeong Lee1,2

  • 1Rheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, 06591, Republic of Korea.

Insights

COVID-19 exacerbates rheumatoid arthritis (RA) by increasing inflammation, autoantibody production, and thrombosis. The SARS-CoV-2 spike protein accelerated RA development and severity in a collagen-induced arthritis mouse model.

Area of Science:

  • Immunology
  • Rheumatology
  • Virology

Background:

  • Coronavirus disease 2019 (COVID-19) shares symptoms with autoimmune diseases like rheumatoid arthritis (RA), including inflammation and thrombosis.
  • The precise impact of COVID-19 on the development and progression of autoimmune conditions remains unclear.

Discussion:

  • In vitro, SARS-CoV-2 spike protein overexpression in human fibroblast-like synoviocytes (FLS) significantly elevated inflammatory cytokine and chemokine expression.
  • In vivo, the SARS-CoV-2 spike protein slightly increased RA incidence and severity in a collagen-induced arthritis (CIA) mouse model.

Key Insights:

  • SARS-CoV-2 spike protein significantly increased autoantibodies (e.g., anti-CXCL4, anti-phospholipid) and thrombotic factors in CIA mice.
  • Joint tissue destruction and inflammatory cytokine levels were markedly elevated in CIA mice following SARS-CoV-2 spike protein exposure.
  • COVID-19 accelerates RA development and progression through heightened inflammation, autoantibody generation, and thrombosis.

Outlook:

  • Further research is warranted to elucidate the mechanisms by which SARS-CoV-2 influences RA pathogenesis.
  • Investigating therapeutic strategies targeting COVID-19-induced inflammation and autoimmunity in RA patients is crucial.
  • Understanding the long-term effects of COVID-19 on individuals with pre-existing autoimmune diseases is essential.
Abstract

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