© 2001 American Heart Association, Inc.
Atherosclerosis and Lipoproteins |
Antibodies to Oxidized LDL in Relation to Carotid Atherosclerosis, Cell Adhesion Molecules, and Phospholipase A2
From the Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska University Hospital, Göteborg University, Gothenburg, Sweden.
Correspondence to Johannes Hulthe, MD, PhD, Wallenberg Laboratory, Fack 16, Sahlgrenska University Hospital, S-413 45 Gothenburg, Sweden. E-mail Johannes.Hulthe{at}wlab.wall.gu.se
Abstract—The role of the humoral immune response to oxidized low density lipoprotein (Ox-LDL) in atherogenesis is unclear and available studies are contradictory. The aims of the present study were (1) to compare antibody titers to modified LDL in a group of patients with hypercholesterolemia (n=102) with those in matched controls (n=102), (2) to analyze whether these titers were related to atherosclerosis development as measured by ultrasound, and (3) to analyze whether these titers were related to soluble cell adhesion molecules and secretory type II phospholipase A2 in plasma. The results showed that male patients with hypercholesterolemia had lower immunoglobulin G (IgG) titers compared with those in healthy controls. In the control group, there was an inverse correlation between intima-media thickness of the carotid artery bulb and IgM titers against Ox-LDL and malondialdehyde-LDL (r=-0.35, P=0.001; and r=-0.31, P=0.003, respectively). In the patient group, however, only weak associations were seen. IgG titers were positively associated with soluble intercellular adhesion molecule-1, soluble E-selectin, and secretory type II phospholipase A2. Taken together, the results of this study support the concept that the humoral immune response against Ox-LDL may be protective in early atherosclerosis. The pattern, however, is complex, and the role of the immune response may differ in different patient groups as well as at different stages of the disease.
Key Words: Ox-LDL • antibodies • atherosclerosis • intima-media thickness • inflammation
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