Expression of the haemorrhage‐associated macrophage in Sickle cell disease

Investigators & Affiliations:

Kim R Quimby1, Eyitayo Fakunle2, Ian R Hambleton1, R Clive Landis1.

1 Chronic Disease Research Centre, Tropical Medicine Research Institute, The University of the West Indies, Bridgetown, Barbados
2 Queen Elizabeth Hospital, Barbados

Funding Obtained:

Cave Hill Postgraduate Research Award Fund – 9.2009 – USD $5000.00

Start Date:

January 2010

End Date:

January 2011


Sickle Cell Disease (SCD) is characterized by intravascular haemolysis. Free plasma haemoglobin (Hb), if not adequately cleared, triggers the production of oxidative free radicals which have been linked to vascular dysfunction. The acute haemolysis which occurs during cardiopulmonary bypass was associated with the induction of the haemoglobin‐scavenging receptor – CD163, and the enzyme responsible for heme catabolism – intracellular (haem‐oxygenase‐1) HO‐1. This mechanism limits the inflammatory and oxidative effects of free Hb. Here we assess this principle of induction in steady‐state SCD with the intention of exploring its association with vascular complications.


This was a case – control study where cases were persons with confirmed HbSS, attending the Haematology Unit of the Queen Elizabeth Hospital and clinically well at the time of investigation. Exclusion criteria include: painful crisis within the preceding month, transfusion of blood products within the preceding 3 months, pregnancy and current use of oral corticosteroids. Controls nominated HbAA ‘friends’ – Hb electrophoresis was performed to confirm status. Monocyte surface CD163 and intracellular HO‐1 was analysed by flow cytometry, and plasma Hp concentration was determined by ELISA. All indices were compared in cases and controls using the paired t‐test after examining variable normality.

Main Results:

There was an unexpected inhibition of the vascular protective CD163high monocyte in SCD. This was coupled with a near depleted Hp concentration.

Expected impact:

The inhibition of CD163 is probably due to the inactivation of the Hpdependent positive feedback mechanism for CD163 expression. Lack of CD163 induction and its scavenging properties may exacerbate the vascular insults associated with SCD.

Next Steps / Future Plans:

The next step was two‐fold:

  • To determine the clinical findings associated with Homozygous Sickle cell disease in th Barbadian Population
  • To investigate the clinical impact of the deficit in the haemoglobin scavenging mechanism in SCD
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