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Dr. Jeremy Pearson
The monocyte plays important roles not only in the development of atherosclerotic lesions (where it is classically recognised as the lipid-filled foam cell and therefore as a Bad Thing), but also in the process of collateral vessel development to protect tissues from ischemic injury (and therefore in this context a Good Thing).
This session presented an excellent update of our knowledge in the field, and particularly highlighted the newer findings that make it clear that there are at least two major subtypes of circulating monocyte which have different roles in the vessel wall. Christian Weber described the contrasting surface markers and properties of the two subtypes, noting that the “patrolling” subtype (CD14 low) probably included the cells originally described as endothelial progenitors (EPC) but now thought to act as “angiogenic monocytes” stimulating new vessel formation by paracrine mediator secretion. The other “inflammatory” subtype (CD14 high), increased in mouse models of atherosclerosis, is likely to be the source of the foam cells.
Wulf Ito focussed on monocyte contribution to collateral vessel formation, though his more recent findings emphasised instead the importance of resident tissue progenitors bearing monocyte markers in the development and stabilisation of collateral vessels.
Goran Hansson provided a more detailed picture of the interaction of macrophages and T cells in the evolution of the atherosclerotic plaque, highlighting his group’s recent findings that the inflammatory mediator leukotriene B4, secreted by the plaque macrophages, contributes to plaque progression and is a novel target – consistent with the genetic findings unexpectedly implicating enzymes of leukotriene synthesis in coronary artery disease risk.
Finally, Johannes Waltenberger showed how the migratory function of monocytes isolated from peripheral blood is impaired in patients with cardiovascular risk factors, and, like endothelial dysfunction in these subjects, can be improved by removing risk factors (smoking) or by statin treatment, suggesting that this test can be used as a further biomarker of risk.
Future work, based on the selective homing and adhesion molecules utilised by the two macrophage subtypes, should lead to identification of better ways selectively to enhance traffic of “Good” monocytes to encourage angiogenesis or collateral vessel formation, and to reduce traffic of “Bad” monocytes into the vessel wall in atherogenesis. However, whether the latter is really a good idea needs to be tested, since it is also clear that the macrophage population present in lesions is dynamic, and prevention of entry leads to rapid depletion of lesion macrophage (and lipid) content.
The monocyte: much more than just an inflammatory cell
This congress report accompanies a presentation given at the ESC Congress 2008. Written by the author himself/herself, this report does not necessarily reflect the opinion of the European Society of Cardiology.
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