RETRACTED: SARS-CoV2 mRNA vaccine intravenous administration induces myocarditis in chronic inflammation

Ha-Eun Jeon1, Seonghyun Lee2,3, Jisun Lee2

  • 1Department of Biomedical Science, Jungwon University, Goesan-gun, Chungbuk, Republic of Korea.

Plos One
|October 10, 2024
PubMed

Insights

Investigating messenger RNA (mRNA) vaccines in mice revealed that intravenous administration, especially with chronic inflammation, can worsen heart inflammation (myocarditis) and increase cardiac damage markers. Further research is needed.

Area of Science:

  • Immunology
  • Cardiology
  • Pharmacology

Background:

  • COVID-19 messenger RNA (mRNA) vaccines were developed for pandemic conditions.
  • Their effects on chronic inflammatory conditions and varying administration routes require investigation.

Purpose of the Study:

  • To investigate the cardiac toxicity and immunogenicity of mRNA vaccines in a mouse model of chronic inflammation.
  • To assess the impact of different injection routes on these effects.

Main Methods:

  • Utilized a mouse model with induced chronic inflammation.
  • Administered mRNA vaccines via intravenous (IV) and potentially other routes (route not specified for comparison).
  • Assessed cardiac inflammation (pericarditis, myocarditis) and measured inflammatory cytokines (IL-1beta, IL-6) and serum troponin I (TnI).

Main Results:

  • Intravenous mRNA vaccination exacerbated cardiac inflammation, including pericarditis and myocarditis, in both healthy and chronically inflamed mice.
  • Immunization led to mild cardiac inflammation and increased IL-1beta and IL-6 levels.
  • IV mRNA vaccination significantly increased serum troponin I in mice with lipopolysaccharide (LPS)-induced chronic inflammation, indicating cardiac damage.

Conclusions:

  • Intravenous mRNA vaccine administration may increase cardiotoxicity in individuals with chronic inflammatory conditions.
  • The injection route significantly influences the cardiac effects of mRNA vaccines.
  • Further research is necessary to elucidate the mechanisms underlying these route-dependent cardiac effects.

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