Annexin A1 Is Associated with Adverse Clinical Outcomes in Patients with COVID-19

Matthias H Busch1,2, Sjoerd A M E G Timmermans1,2, Joop P Aendekerk2

  • 1Department of Nephrology and Clinical Immunology, Maastricht University Medical Center, 6202AZ Maastricht, The Netherlands.

Insights

In severe COVID-19, Annexin A1 (AnxA1) levels were higher but showed an insufficient increase, indicating a potential role in disease severity and thrombotic events. This suggests AnxA1 may be a target for future therapeutic interventions.

Area of Science:

  • Immunology
  • Vascular Biology
  • Infectious Diseases

Background:

  • Severe COVID-19 involves hyperinflammation, vascular damage, and hypercoagulability.
  • Annexin A1 (AnxA1) is a pro-resolving protein that inhibits neutrophil activity.
  • Insufficient AnxA1 response may contribute to severe COVID-19 progression.

Purpose of the Study:

  • To longitudinally evaluate the role of AnxA1 in inflammation, vascular damage, and clinical outcomes in COVID-19 patients.
  • To assess AnxA1 levels in relation to disease severity and thrombotic events.
  • To investigate the dynamic changes of AnxA1 during the course of COVID-19.

Main Methods:

  • Prospective cohort study of 220 COVID-19 patients during the first wave.
  • Longitudinal measurement of serum AnxA1 at presentation and follow-up.
  • Statistical analyses including multivariable logistic regression and linear mixed models.

Main Results:

  • AnxA1 levels were significantly higher in moderate/severe COVID-19 cases versus healthy controls.
  • Elevated AnxA1 correlated with inflammation markers and endothelial damage.
  • Higher AnxA1 was associated with thrombotic events and ICU admission; baseline AnxA1 predicted thrombosis.
  • AnxA1 showed a steeper increase over time in patients without adverse events, suggesting an insufficient response in severe cases.

Conclusions:

  • Findings suggest an insufficient AnxA1 response to hyperinflammation in severe COVID-19.
  • AnxA1's role in disease severity and thrombosis warrants further investigation.
  • AnxA1 or its peptide Ac2-26 may be potential therapeutic targets for reducing hyperinflammation.

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