Leucocyte-bound apolipoprotein B in the circulation is inversely associated with the presence of clinical and subclinical atherosclerosis.
BACKGROUND
Atherosclerosis is a pro-inflammatory condition, in which leucocyte activation plays an important role. The interaction between circulating leucocytes and apolipoprotein (apo) B-containing lipoproteins results in pro-inflammatory changes of these cells. We aimed to evaluate the relationship between apo B bound to circulating leucocytes and atherosclerosis.


METHODS
Apo B on circulating leucocytes was measured by flow cytometry in subjects with and without cardiovascular disease (CVD), expressed as mean fluorescent intensity in arbitrary units (au). Carotid intima-media thickness (cIMT) was measured using B-mode ultrasound. Data are given as median (interquartile range).


RESULTS
A total of 396 subjects were included, of whom 183 had a history of CVD. Compared to subjects without CVD, patients with CVD had lower apo B bound to neutrophils (12·7 au (9·8-16·2) and 14·2 au (10·1-17·5), respectively, P = 0·038) and to monocytes (2·5 au (1·7-3·1) and 2·7 (1·9-3·6) au, respectively, P = 0·025). No differences were found for lymphocyte-bound apo B. Neutrophil- and monocyte-bound apo B were inversely correlated with cIMT (Spearman's rho: -0·123, P = 0·017 and -0·108, P = 0·035, respectively). Both monocyte- and neutrophil-bound apo B were inversely associated with different factors related to the metabolic syndrome, such as body mass index, triglycerides and complement C3. There was a positive association between erythrocyte-bound apo B and apo B bound to each of the leucocyte classes, possibly reflecting a similar mechanism. Discontinuation of statins in 54 subjects did not influence leucocyte-bound apo B.


CONCLUSIONS
Unexpectedly, the presence of noninternalized apo B-containing lipoproteins on circulating neutrophil and monocyte membranes may represent a protective mechanism against atherosclerosis.
Department of Internal Medicine, Center for Diabetes and Vascular Medicine, St. Franciscus Gasthuis, Rotterdam, The Netherlands.
Marijke A
MA
de Vries
Department of Internal Medicine, Center for Diabetes and Vascular Medicine, St. Franciscus Gasthuis, Rotterdam, The Netherlands.
Boudewijn
B
Klop
Department of Internal Medicine, Center for Diabetes and Vascular Medicine, St. Franciscus Gasthuis, Rotterdam, The Netherlands.
Noëlle
N
van der Meulen
Department of Clinical Chemistry, St. Franciscus Gasthuis, Rotterdam, The Netherlands.
Gert-Jan M
GJ
van de Geijn
Department of Clinical Chemistry, St. Franciscus Gasthuis, Rotterdam, The Netherlands.
Lenneke
L
Prinzen
Department of Clinical Chemistry, St. Franciscus Gasthuis, Rotterdam, The Netherlands.
Ellen
E
van der Zwan
Department of Statistics and Education, St. Franciscus Gasthuis, Rotterdam, The Netherlands.
Erwin
E
Birnie
Department of Statistics and Education, St. Franciscus Gasthuis, Rotterdam, The Netherlands.
Jan W
JW
Cohen Tervaert
Department of Cardiology, St. Franciscus Gasthuis, Rotterdam, The Netherlands.
Anho H
AH
Liem
Department of Endocrinology, Erasmus Medical Center, Rotterdam, The Netherlands.
Wouter W
WW
de Herder
Department of Internal Medicine, Center for Diabetes and Vascular Medicine, St. Franciscus Gasthuis, Rotterdam, The Netherlands.
Manuel
M
Castro Cabezas
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001055:Apolipoproteins B / Q000378:metabolism*; D050197:Atherosclerosis / Q000188:drug therapy / Q000209:etiology*; D059168:Carotid Intima-Media Thickness; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007962:Leukocytes / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism; D012307:Risk Factors; D055815:Young Adult
D001055:Apolipoproteins B; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors
Coronary artery disease; inflammation; intima-media thickness; leucocyte activation; monocyte; neutrophil