Sulicka-Grodzicka Joanna, Surdacki Andrzej, Surmiak Marcin, Sanak Marek, Wizner Barbara, Sydor Wojciech, Bociąga-Jasik Monika, Strach Magdalena, Korkosz Mariusz, Skladany Lubomir, Grgurevic Ivica, Podrug Kristian, Kukla Michał
Department of Rheumatology and Immunology, Jagiellonian University Medical College, 30-688 Cracow, Poland.
Institute of Cardiology, Jagiellonian University Medical College, 30-688 Cracow, Poland.
Biomedicines. 2022 Oct 1;10(10):2462. doi: 10.3390/biomedicines10102462.
Chemerin is one of the specialized pro-resolving mediators that participate in the early phase of inflammation and contribute to the initiation of the pro-resolving response. There is a paucity of data regarding the time course of chemerin during acute infections. We aimed to evaluate the sequence of inflammatory responses in the acute COVID-19 phase throughout onset and resolution of inflammation. We evaluated changes in selected biomarkers in COVID-19 survivors on the 7-day and 28-day follow up. Chemerin was lower in patients with baseline moderate/severe disease at day 7 compared with asymptomatic patients and individuals with mild illness (7265 [5526−9448] vs. 8730 [6888−11,058] pg/mL; p = 0.03). Only in patients with moderate/severe disease, but not in those with mild symptoms, were chemerin concentrations decreased one week after infection onset compared with baseline (7265 [5526−9448] vs. 8866 [6383−10,690] pg/mL; p < 0.05) with a subsequent increase on the 28-day follow up (9313 [7353−11,033] pg/mL; p < 0.05). Resolution of inflammation in the group of moderate/severe SARS-CoV2 infection was associated with increasing serum concentrations of chemerin, contrary to pro-inflammatory cytokines and adipokines (pentraxin 3, TNFα, resistin, leptin). A similar pattern of angiopoietin-2 dynamics may suggest signs of enhanced vascularization as a consequence of acute SARS-CoV2 infection.
凯莫瑞蛋白是参与炎症早期阶段并促成促消退反应启动的特异性促消退介质之一。关于急性感染期间凯莫瑞蛋白的时间进程，数据匮乏。我们旨在评估急性新冠肺炎阶段从炎症发作到消退整个过程中的炎症反应序列。我们在7天和28天随访时评估了新冠肺炎幸存者中选定生物标志物的变化。与无症状患者和轻症患者相比，基线为中度/重度疾病的患者在第7天时凯莫瑞蛋白水平较低（7265 [5526−9448] 对8730 [6888−11,058] pg/mL；p = 0.03）。仅在中度/重度疾病患者中，而非轻症患者中，感染发作一周后与基线相比凯莫瑞蛋白浓度降低（7265 [5526−9448] 对8866 [6383−10,690] pg/mL；p < 0.05），随后在28天随访时升高（9313 [7353−11,033] pg/mL；p < 0.05）。与促炎细胞因子和脂肪因子（五聚素3、肿瘤坏死因子α、抵抗素、瘦素）相反，中度/重度SARS-CoV2感染组炎症的消退与血清凯莫瑞蛋白浓度升高相关。血管生成素-2动态变化的类似模式可能提示急性SARS-CoV2感染导致血管生成增强的迹象。
