C-reactive protein (CRP), an acute-phase reactant, is a significant risk factor for coronary heart disease. This study demonstrates that CRP directly induces the expression of adhesion molecules in human endothelial cells, potentially contributing to atherosclerosis. CRP significantly increased the expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in human umbilical vein endothelial cells (HUVECs) and coronary artery endothelial cells (HCAECs) when cultured in the presence of human serum. The effect was dose-dependent, with maximum induction at 50 μg/mL for ICAM-1 and VCAM-1, and significant E-selectin expression at higher concentrations. CRP's effect was dependent on the presence of human serum, as serum-free medium did not elicit a response. In contrast, interleukin-1β could induce adhesion molecule expression without serum. These findings suggest that CRP may play a direct role in promoting the inflammatory component of atherosclerosis. The study also shows that CRP can induce adhesion of monocytic cells to endothelial cells, indicating a proinflammatory effect. CRP levels are elevated in unstable angina and acute myocardial infarction, and higher levels are associated with increased risk of coronary events. The study highlights that CRP may not only be a marker of inflammation but also have a direct role in atherosclerosis pathogenesis. Lowering CRP levels may reduce atherosclerosis progression and coronary events. The mechanisms of CRP's proinflammatory effects on endothelial cells are not fully understood, but they appear to depend on serum components. Further research is needed to elucidate these mechanisms. In conclusion, CRP induces significant expression of adhesion molecules in human endothelial cells, suggesting it may contribute to the development and progression of atherosclerosis.C-reactive protein (CRP), an acute-phase reactant, is a significant risk factor for coronary heart disease. This study demonstrates that CRP directly induces the expression of adhesion molecules in human endothelial cells, potentially contributing to atherosclerosis. CRP significantly increased the expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in human umbilical vein endothelial cells (HUVECs) and coronary artery endothelial cells (HCAECs) when cultured in the presence of human serum. The effect was dose-dependent, with maximum induction at 50 μg/mL for ICAM-1 and VCAM-1, and significant E-selectin expression at higher concentrations. CRP's effect was dependent on the presence of human serum, as serum-free medium did not elicit a response. In contrast, interleukin-1β could induce adhesion molecule expression without serum. These findings suggest that CRP may play a direct role in promoting the inflammatory component of atherosclerosis. The study also shows that CRP can induce adhesion of monocytic cells to endothelial cells, indicating a proinflammatory effect. CRP levels are elevated in unstable angina and acute myocardial infarction, and higher levels are associated with increased risk of coronary events. The study highlights that CRP may not only be a marker of inflammation but also have a direct role in atherosclerosis pathogenesis. Lowering CRP levels may reduce atherosclerosis progression and coronary events. The mechanisms of CRP's proinflammatory effects on endothelial cells are not fully understood, but they appear to depend on serum components. Further research is needed to elucidate these mechanisms. In conclusion, CRP induces significant expression of adhesion molecules in human endothelial cells, suggesting it may contribute to the development and progression of atherosclerosis.