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Inflammatory role of platelets in acute coronary syndromes
  1. Section of Clinical Immunology and Infectious Diseases
  2. Research Institute for Internal Medicine
  3. Department of Cardiology
  4. Rikshospitalet
  5. N-0027 Oslo
  6. Norway
  1. Dr Aukrust;pal.aukrust{at}

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Increasing evidence shows that inflammatory mediators play a pathogenic role in atherogenesis and acute coronary syndrome.1 In particular, several reports suggest that inflammatory cytokines such as tumour necrosis factor α (TNFα), interleukin (IL)-1 and various chemokines (for example, IL-8) may enhance degradation of the connective tissue matrix protein by activating matrix metalloproteinases (MMPs) and induce apoptosis of cells within the atherosclerotic lesion, promoting plaque destabilisation and rupture.1 2 These findings indicate a pathogenic link between persistent immune activation and plaque rupture in coronary artery disease. It is well established that platelets also contribute to the pathogenesis of acute coronary syndromes by promoting thrombus formation. However, recent studies suggest that these cells also may trigger an acute coronary event through other mechanisms, such as stimulation of an inflammatory response within the atherosclerotic plaque.

Platelets as inflammatory cells

Several lines of evidence support a role for platelets as inflammatory cells. Firstly, platelets provide a wide range of growth factors and inflammatory mediators by their release from intracellular storage organelles. Included in this group of mediators are several members of the chemokine family. In fact, platelet factor 4 and β-thromboglobulin, localised in platelet α-granules, represented the first chemokines to be discovered.3 In recent years, a number of CC- and CXC- as well as other cytokines—for example, CD40 ligand (CD40L)—have been found in these cells.3 4Second, platelets do not only contain and express inflammatory mediators, but may upon activation also induce the expression of such substances (for example, TNFα and chemokines) in monocytes/macrophages. Actually, upon activation platelets express P-selectin on their surface. Through ligation with its counterpart on monocytes/macrophages, …

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