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Low mannose-binding lectin and increased complement activation correlate to allograft vasculopathy, ischaemia, and

Arnt E Fiane1, Thor Ueland, Svein Simonsen

  • 1Department of Thoracic and Cardiovascular Surgery, Rikshospitalet University Hospital, N-0027 Oslo, Norway.

European Heart Journal
|April 12, 2005
PubMed

Insights

Low mannose-binding lectin (MBL) levels are linked to transplant-associated coronary artery disease (TxCAD) and acute rejection after heart transplants. Increased complement activation also correlates with ischemia and mortality in these patients.

Area of Science:

  • Immunology
  • Transplantation Medicine
  • Cardiology

Background:

  • Transplant-associated coronary artery disease (TxCAD) is a primary cause of graft failure following heart transplantation.
  • Mannose-binding lectin (MBL) and complement activation are implicated in inflammatory and immune responses.
  • Understanding the role of MBL and complement in TxCAD is crucial for improving long-term transplant outcomes.

Purpose of the Study:

  • To investigate the association between MBL deficiency, complement activation, and the development of TxCAD.
  • To explore the relationship between MBL levels, acute rejection episodes, and endothelial activation markers.
  • To determine the correlation of complement activation and terminal complement complex with histopathologic ischemia and mortality post-heart transplant.

Main Methods:

  • Prospective study of 38 heart transplant recipients with a mean follow-up of 5.3 years.
  • Assessment of plasma MBL levels, complement activation markers (C4bc, terminal complement complex), and endothelial activation (soluble E-selectin).
  • Correlation analysis between these markers, angiographically verified TxCAD, acute rejection episodes, and patient mortality.

Main Results:

  • MBL deficiency (<100 ng/mL) was significantly associated with TxCAD (P=0.020) and a higher incidence of acute rejection episodes (P=0.016).
  • Complement activation (C4bc) and soluble E-selectin levels were significantly elevated in patients with histopathologic ischemia (P=0.037 and P=0.002, respectively).
  • Terminal complement complex levels showed a strong correlation with patient mortality (P=0.002).

Conclusions:

  • Low MBL levels are a risk factor for TxCAD and acute rejection after heart transplantation.
  • Increased complement activation is linked to histopathologic ischemia and predicts mortality.
  • Targeting MBL and complement pathways may offer therapeutic strategies to prevent TxCAD and improve graft survival.
Abstract

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