Enhanced inflammatory response of blood monocytes to C-reactive protein in patients with unstable angina

• Published in: Clinica chimica acta Vol. 352; no. 1; pp. 127 - 133
• Main Authors: Li, Jian-Jun, Wang, Hai-Rong, Huang, Cong-Xin, Xue, Jia-Lin, Li, Geng-Shan
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.02.2005
• Subjects: Adjuvants, Immunologic - blood; Adjuvants, Immunologic - physiology; Aged; Angina, Unstable - blood; Angina, Unstable - immunology; C-reactive protein; C-Reactive Protein - metabolism; C-Reactive Protein - physiology; Female; Humans; Inflammation Mediators - blood; Inflammation Mediators - physiology; Interleukin-6; Male; Middle Aged; Monocyte; Monocytes - metabolism; tnf-α; Unstable angina; C-reactive protein; Monocyte; tnf-α; Unstable angina; Interleukin-6
• ISSN: 0009-8981; 1873-3492
• DOI: 10.1016/j.cccn.2004.08.019

Previous studies showed that monocytes from patients with unstable coronary disease exhibit a greatly enhanced production of interleukin-6 (IL-6) in response to lipopolysaccharide and artery injury. Moreover, accumulating evidence suggest that C-reactive protein (CRP) may have direct proinflammatory effects on the cells of vascular wall. Whether this enhanced inflammatory response also exists, however, in cultured monocytes from patients with unstable angina, in response to CRP, has not been investigated. Monocytes were isolated from blood of 15 healthy volunteers (normal control), 15 patients with stable angina, and 15 patients with unstable angina by Ficoll density gradient and were stimulated by 20 μg/ml of CRP for 24 h. Measurements of IL-6 and tumor necrosis factor-a (tnf-α) were performed from supernatants of cultured medium in duplicate, using a commercial assay kit. Results: the data showed that IL-6 and tnf-α concentrations of spontaneous secretion (baseline) were higher in patients with unstable angina than in patients with stable angina and normal control (IL-6: 179±19 vs. 87±6 and 89±8 pg/ml, p<0.05, respectively; tnf-α: 69±13 vs. 30±4 and 27±3 pg/ml, p<0.05, respectively). CRP induced the enhanced release of IL-6 and tnf-α by 17-fold and 23-fold increase, respectively, in patients with unstable angina, while it did about 11-fold and 19-fold increase in patients with stable angina and normal group (IL-6: 3129±333 vs. 991±134 and 987±102 pg/ml, p<0.01, respectively; tnf-α: 1554±784 vs. 560±135 and 558±152 pg/ml, p<0.01, respectively). Increased baseline concentrations of IL-6 and tnf-α can be a marker of the hyperresponsiveness of the inflammatory system in patients with unstable coronary disease. CRP could enhance even further this response, suggesting that a persisted and enhanced inflammatory responsiveness to CRP may be involved in the pathogenesis of unstable coronary disease.