Horváth Z, Csuka D, Vargova K, Leé S, Varga L, Garred P, Préda I, Zsámboki E T, Prohászka Z, Kiss R G
Research Group for Inflammation Biology and Immunogenomics of Hungarian Academy of Sciences and Semmelweis University, Budapest, Hungary.
Department of Cardiology, Hungarian Defence Forces Medical Centre, Budapest, Hungary.
Scand J Immunol. 2016 Sep;84(3):174-81. doi: 10.1111/sji.12454.
In patients with typical angina pectoris, inducible myocardial ischaemia and macroscopically normal coronaries (cardiac syndrome X (CSX)), a significantly elevated plasma level of terminal complement complex (TCC), the common end product of complement activation, has been observed without accompanying activation of the classical or the alternative pathways. Therefore, our aim was to clarify the role of the ficolin-lectin pathway in CSX. Eighteen patients with CSX, 37 stable angina patients with significant coronary stenosis (CHD) and 54 healthy volunteers (HC) were enrolled. Serum levels of ficolin-2 and ficolin-3, ficolin-3/MASP-2 complex and ficolin-3-mediated TCC deposition (FCN3-TCC) were determined. Plasma level of TCC was significantly higher in the CSX than in the HC or CHD group (5.45 versus 1.30 versus 2.04 AU/ml, P < 0.001). Serum levels of ficolin-2 and ficolin-3 were significantly lower in the CSX compared to the HC or CHD group (3.60 versus 5.80 or 5.20 μg/ml, P < 0.05; 17.80 versus 24.10 or 26.80 μg/ml, P < 0.05). The ficolin-3/MASP-2 complex was significantly lower in the CSX group compared to the HC group (92.90 versus 144.90 AU/ml, P = 0.006). FCN3-TCC deposition was significantly lower in the CSX group compared to the HC and CHD groups (67.8% versus 143.3% or 159.7%, P < 0.05). In the CSX group, a significant correlation was found between TCC and FCN3-TCC level (r = 0.507, P = 0.032) and between ficolin-3/MASP-2 complex level and FCN3-TCC deposition (r = 0.651, P = 0.003). In conclusion, in patients with typical angina and myocardial ischaemia despite macroscopically normal coronary arteries, low levels of several lectin pathway parameters were observed, indicating complement activation and consumption. Complement activation through the ficolin-lectin pathway might play a role in the complex pathomechanism of CSX.
在患有典型心绞痛、可诱导性心肌缺血且冠状动脉在宏观上正常（心脏综合征X（CSX））的患者中，已观察到补体激活的共同终产物——终末补体复合物（TCC）的血浆水平显著升高，而经典途径或替代途径并未伴随激活。因此，我们的目的是阐明纤维胶凝蛋白-凝集素途径在CSX中的作用。纳入了18例CSX患者、37例患有严重冠状动脉狭窄的稳定型心绞痛患者（冠心病（CHD））和54名健康志愿者（HC）。测定了纤维胶凝蛋白-2和纤维胶凝蛋白-3、纤维胶凝蛋白-3/MASP-2复合物的血清水平以及纤维胶凝蛋白-3介导的TCC沉积（FCN3-TCC）。CSX组的TCC血浆水平显著高于HC组或CHD组（5.45对1.30对2.04 AU/ml，P<0.001）。与HC组或CHD组相比，CSX组的纤维胶凝蛋白-2和纤维胶凝蛋白-3血清水平显著降低（3.60对5.80或5.20μg/ml，P<0.05；17.80对24.10或26.80μg/ml，P<0.05）。与HC组相比，CSX组的纤维胶凝蛋白-3/MASP-2复合物显著降低（92.90对144.90 AU/ml，P=0.006）。与HC组和CHD组相比，CSX组的FCN3-TCC沉积显著降低（67.8%对143.3%或159.7%，P<0.05）。在CSX组中，发现TCC与FCN3-TCC水平之间存在显著相关性（r=0.507，P=0.032），纤维胶凝蛋白-3/MASP-2复合物水平与FCN3-TCC沉积之间也存在显著相关性（r=0.651，P=0.003）。总之，在患有典型心绞痛和心肌缺血但冠状动脉在宏观上正常的患者中，观察到几种凝集素途径参数水平较低，表明补体激活和消耗。通过纤维胶凝蛋白-凝集素途径的补体激活可能在CSX复杂的发病机制中起作用。
