Author(s): Sato T, Kameyama T, Noto T, Inoue H
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Abstract BACKGROUND: Coronary intraplaque hemorrhage (IPH) accelerates atherosclerosis. Extracellular hemoglobin (Hb) released by IPH is cleared by macrophages with CD163 receptors. This process provokes secretion of the anti-atherosclerotic cytokine interleukin (IL)-10. The present study aimed to investigate the relationship between macrophage accumulation and IL-10 production provoked by IPH in plaques obtained from acute coronary syndrome (ACS) patients with hyperglycemia. METHODS: In 50 ACS patients, atherothrombotic debris was retrieved during percutaneous coronary intervention (PCI). The debris was stained with antibodies to CD163, glycophorin A (GPA, a marker of IPH) and IL-10. \%CD163 was defined as the ratios of CD163-positive cells to all cells. \%IL-10 and \%GPA were defined as the ratio of positively stained areas per total tissue area. Based on glycosylated Hb [HbA1c (NGSP)] ≥ 6.5\%, fasting blood sugar (FBS) ≥ 126 mg/dL, and insulin resistance (HOMA-IR>2.5), patients were divided into a diabetes mellitus (DM) group (N = 18, HbA1c ≥ 6.5\% or FBS ≥ 126 mg/dL), an insulin resistance (IR) group (N = 15, HOMA-IR>2.5, HbA1c<6.5\%, and FBS< 126 mg/dL), and a normal (NR) group (N = 17). RESULTS: Compared to the NR group, \%GPA and \%CD163 were increased in the DM and IR groups. \%IL-10 was similar among the three groups. However, \%IL-10/\%CD163 ratios were decreased in the DM (2.5 ± 0.6, P = 0.01) and IR (2.7 ± 0.8, P = 0.02) groups compared to the NR group (5.8 ± 4.7). Only in the NR group was there a significant correlation between \%IL-10 and \%CD163. CONCLUSIONS: Impairment of the anti-inflammatory effect provoked by IPH contributes to premature atherosclerosis even in the IR group. © 2014.
This article was published in J Diabetes Complications
and referenced in Journal of Microbial & Biochemical Technology