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Increased expression of CD11b/CD18 on phagocytes in ischaemic disease: a bridge between inflammation and coagulation
Author(s) -
MAZZONE A.,
DE SERVI S.,
MAZZUCCHELLI I.,
FOSSATI G.,
GRITTI D.,
CANALE C.,
CUSA C.,
RICEVUTI G.
Publication year - 1997
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.1997.1610710.x
Subject(s) - cd18 , integrin alpha m , medicine , cell adhesion molecule , inflammation , coronary artery disease , immunology , flow cytometry , gastroenterology
The aim of this study was to assess the expression of CD11b/CD18 integrin adhesion molecules on the phagocytes of patients with ischaemic diseases, and to evaluate the concentration of soluble adhesion molecules that are released from endothelium (sICAM‐1) and from phagocytes (sL‐selectin). A total of 370 patients were enrolled: 120 with coronary artery disease (CAD); 50 with peripheral artery occlusive disease (PAOD); and 200 control subjects with no clinical manifestations of ischaemic disease. CD11b/CD18 integrin was detected by flow cytometry, whereas sL‐selectin and sICAM‐1 concentrations were detected using a sandwich‐type immunoassay. CD11b/CD18 integrin expression was found to be higher in the patients with ischaemic disease than in the control subjects ( P < 0.001). The PAOD patients had higher values of CD11b/CD18 integrin than the CAD ones ( P < 0.01). The concentration of soluble adhesion molecules did not show any significant differences within the three groups ( P = NS). The high expression of CD11b/CD18 integrin in ischaemic disease patients may depend on the increased, but probably stable, cytokine network that has been demonstrated to occur in chronic ischaemic diseases: the difference observed between PAOD and CAD patients could be the consequence of higher inflammatory activation probably resulting from the greater extent of the atherosclerotic process in PAOD, or of the more localized ischaemic area in CAD patients. CD11b/CD18 can therefore be considered a marker of chronic phagocyte activation during ischaemic disease. On the other hand, sICAM and sL‐selectin concentrations were found to be within the normal range; they have recently been considered as a marker for acute ischaemic events and acute inflammatory process activation. Our results confirm that in uncomplicated atherosclerosis no acute inflammatory process activation should occur.