Skowasch Dirk, Tuleta Izabela, Steinmetz Martin, Pabst Stefan, Preusse Claus J, Welz Armin, Nickenig Georg, Bauriedel Gerhard
Department of Internal Medicine II - Cardiology, University of Bonn, Bonn, Germany.
J Heart Valve Dis. 2009 Jul;18(4):411-7.
The presence of five pathogens was assessed, together with a possible correlation of the total pathogen burden on inflammation and (auto)immunity in aortic stenosis (AS) and degenerative aortic valve bioprosthesis (BP).
Diseased valve specimens from a total of 68 patients (52 with AS, 16 with BP) were studied. The presence and localization was assessed of Chlamydia pneumoniae (cHSP60), Helicobacter pylori (HP), cytomegalovirus (CMV), Epstein-Barr virus (EBV) and herpes simplex virus (HSV), as well as of macrophages (CD68), C-reactive protein (CRP) and human heat shock protein 60 (hHSP60), by using immunohistochemical and morphometric analyses.
In the majority of degenerative aortic valves, specific pathogens, inflammation and immunity were localized predominantly in the fibrosa of AS patients, and in superficial regions of the BP. The categorization of valves as having four or more pathogens (n = 37) or fewer pathogens (n = 31) demonstrated an increased signaling of CD68 (p = 0.03) and CRP (p = 0.02). Specifically, cHSP60, HP and hHSP60 levels were increased in valves where one or two bacteria were identified (n = 59) compared to those without bacterial presence (n = 9) (p = 0.04).
The pathogen burden may contribute to valvular degeneration by promoting further deleterious inflammatory and (auto)immune processes at the level of the valvular fibrosa.
评估了五种病原体的存在情况,以及主动脉瓣狭窄(AS)和退行性主动脉瓣生物假体(BP)中病原体总负荷与炎症和(自身)免疫之间可能存在的相关性。
对总共68例患者(52例AS患者,16例BP患者)的病变瓣膜标本进行了研究。通过免疫组织化学和形态计量分析,评估了肺炎衣原体(cHSP60)、幽门螺杆菌(HP)、巨细胞病毒(CMV)、爱泼斯坦-巴尔病毒(EBV)和单纯疱疹病毒(HSV)以及巨噬细胞(CD68)、C反应蛋白(CRP)和人热休克蛋白60(hHSP60)的存在和定位。
在大多数退行性主动脉瓣中,特定病原体、炎症和免疫主要定位于AS患者的纤维层以及BP的表层区域。将瓣膜分为有四种或更多病原体(n = 37)或较少病原体(n = 31)两类,结果显示CD68(p = 0.03)和CRP(p = 0.02)的信号增强。具体而言,与未检测到细菌的瓣膜(n = 9)相比,在检测到一两种细菌的瓣膜(n = 59)中,cHSP60、HP和hHSP60水平升高(p = 0.04)。
病原体负荷可能通过在瓣膜纤维层水平促进进一步有害的炎症和(自身)免疫过程,从而导致瓣膜退变。