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Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma
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SARS-CoV-2 spike protein accelerates systemic sclerosis by increasing inflammatory cytokines, Th17 cells, and

Ha Yeon Jeong1,2,3, Jin-Sil Park1,2, Jin Seok Woo1,2

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

Journal of Inflammation (London, England)
|December 22, 2023
PubMed

Insights

The SARS-CoV-2 spike protein may worsen systemic sclerosis (SSc) by increasing fibrosis, inflammation, autoantibody production, and thrombosis. This research explores the link between COVID-19 and SSc progression.

Area of Science:

  • Immunology
  • Rheumatology
  • Virology

Background:

  • Coronavirus disease 2019 (COVID-19) shares symptoms with autoimmune diseases like systemic sclerosis (SSc).
  • The precise impact of COVID-19 on SSc remains unclear, despite a case report suggesting a link.

Purpose of the Study:

  • To investigate the effects of the SARS-CoV-2 spike protein on systemic sclerosis (SSc).
  • To elucidate the mechanisms by which COVID-19 might influence SSc development and progression.

Main Methods:

  • In vitro analysis of fibrosis markers in HEK293 cells transfected with SARS-CoV-2 spike protein.
  • In vivo study using a bleomycin-induced SSc mouse model exposed to the SARS-CoV-2 spike protein and ACE2 receptor.
  • Assessment of fibrosis, autoantibodies, thrombotic factors, and inflammatory cytokines.

Main Results:

  • Elevated fibrosis markers in vitro; increased skin thickness and fibrosis in SSc mice exposed to the spike protein.
  • Significant increases in autoantibodies (including anti-phospholipid antibodies) and thrombotic factors observed.
  • Upregulation of the pro-inflammatory cytokine IL-17 and exacerbated tissue fibrosis and inflammation in SSc mice.

Conclusions:

  • COVID-19 may accelerate SSc by intensifying fibrosis.
  • The acceleration is potentially mediated by increased inflammation, autoantibody production, and thrombosis.
  • The SARS-CoV-2 spike protein appears to play a key role in exacerbating SSc pathology.
Abstract

Keywords:
Autoimmune DiseaseCoronavirus Disease 2019 (COVID-19)FibrosisInflammationSystemic sclerosis

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