Pathology Unit, L. Sacco Department of Clinical Sciences, L. Sacco Hospital, Università degli Studi di Milano, Milan, Italy.
Cardiovasc Pathol. 2011 Jan-Feb;20(1):e27-35. doi: 10.1016/j.carpath.2010.02.005. Epub 2010 Mar 30.
The long pentraxin 3 is involved in innate resistance to pathogens, controlling inflammation and extracellular matrix remodeling. Moreover, pentraxin 3 plays a nonredundant role in the regulation of cardiac tissue damage in mice and, recently, it has been proposed as a new candidate marker for acute and chronic heart diseases. However, the actual localization and cellular sources of pentraxin 3 in ischemic and infectious cardiac pathology have not been carefully defined.
In this study, using immunohistochemistry, we analyzed pentraxin 3 expression in the heart tissues of patients with acute myocardial infarction at different time points after the ischemic event. In addition, we studied the heart tissues of patients with infectious myocarditis (fungi, bacteria, and protozoa) and patients who died of noncardiac events with normal heart histology.
In acute myocardial infarction cases, we observed pentraxin 3 localized within and around ischemic lesions. On the contrary, no pentraxin 3 was observed in normal heart areas. In early ischemic lesions, pentraxin 3 was localized primarily in granulocytes; in more advanced acute myocardial infarction, pentraxin 3 positivity was found in the interstitium and in the cytoplasm of macrophages and the endothelium, whereas most granulocytes did not express pentraxin 3, presumably as a consequence of degranulation. In infectious myocarditis, pentraxin 3 was present and localized within and around histological lesions, associated with macrophage, endothelial cell, and, more rarely, myocardiocyte and granulocyte positivities. As observed in acute myocardial infarction patients, no pentraxin 3 staining was found in normal heart areas.
Thus, neutrophils are an early source of pentraxin 3 in acute myocardial infarction and presumably other inflammatory heart disorders. Subsequently, in acute myocardial infarction and infectious myocarditis, pentraxin 3 is produced by macrophages, the endothelium, and, to a lesser extent, myocardiocytes, and localized in the interstitium.
长型五聚素 3 参与先天病原体抵抗,控制炎症和细胞外基质重塑。此外,五聚素 3 在调节小鼠心脏组织损伤方面发挥着非冗余作用,最近它被提议作为急性和慢性心脏病的新候选标志物。然而,五聚素 3 在缺血性和感染性心脏病中的实际定位和细胞来源尚未被仔细定义。
在这项研究中,我们使用免疫组织化学分析了不同时间点缺血性事件后急性心肌梗死患者心脏组织中五聚素 3 的表达。此外,我们还研究了真菌感染、细菌感染和原生动物感染性心肌炎患者以及因非心脏原因死亡但心脏组织正常的患者的心脏组织。
在急性心肌梗死病例中,我们观察到五聚素 3 定位于缺血性病变的内部和周围。相反,在正常心脏区域未观察到五聚素 3。在早期缺血性病变中,五聚素 3 主要定位于粒细胞中;在更晚期的急性心肌梗死中,五聚素 3 阳性位于间质中以及巨噬细胞和内皮细胞的细胞质中,而大多数粒细胞不表达五聚素 3,可能是脱颗粒的结果。在感染性心肌炎中,五聚素 3 存在并定位于组织学病变的内部和周围,与巨噬细胞、内皮细胞以及更罕见的心肌细胞和粒细胞阳性相关。如在急性心肌梗死患者中观察到的,在正常心脏区域未发现五聚素 3 染色。
因此,中性粒细胞是急性心肌梗死和推测其他炎症性心脏病中五聚素 3 的早期来源。随后,在急性心肌梗死和感染性心肌炎中,五聚素 3 由巨噬细胞、内皮细胞产生,并且在较小程度上由心肌细胞产生,并定位于间质中。