Xiao Zhiqing, Lin Minggui, Song Ning, Wu Xue, Hou Jingyu, Wang Lili, Tian XinLun, An Chunge, Dela Cruz Charles S, Sharma Lokesh, Chang De
Department of Pulmonary and Critical Care Medicine at The Seventh Medical Center, College of Pulmonary and Critical Care Medicine of The Eighth Medical Center, Chinese PLA General Hospital, Beijing 100853, China.
Hebei North University, Zhangjiakou 075000, Hebei, China.
iScience. 2024 May 25;27(6):110110. doi: 10.1016/j.isci.2024.110110. eCollection 2024 Jun 21.
Increased cases of sepsis during COVID-19 in the absence of known bacterial pathogens highlighted role of viruses as causative agents of sepsis. In this study, we investigated clinical, laboratory, proteomic, and metabolomic characteristics of viral sepsis patients ( = 45) and compared them to non-sepsis patients with COVID-19 ( = 186) to identify molecular mechanisms underlying the pathology of viral sepsis in COVID-19. We identified unique metabolomic and proteomic signatures that suggest a substantial perturbation in the coagulation, complement, and platelet activation pathways in viral sepsis. Our proteomic data indicated elevated coagulation pathway protein (fibrinogen), whereas a decrease in many of the complement proteins was observed. These alterations were associated with the functional consequences such as susceptibility to secondary bacterial infections and potentially contributing to both local and systemic disease phenotypes. Our data provide novel aspect of COVID-19 pathology that is centered around presence of sepsis phenotype in COVID-19.
在没有已知细菌病原体的情况下，COVID-19期间脓毒症病例增加，这凸显了病毒作为脓毒症病原体的作用。在本研究中，我们调查了病毒性脓毒症患者（n = 45）的临床、实验室、蛋白质组学和代谢组学特征，并将其与COVID-19非脓毒症患者（n = 186）进行比较，以确定COVID-19中病毒性脓毒症病理的分子机制。我们确定了独特的代谢组学和蛋白质组学特征，表明病毒性脓毒症中凝血、补体和血小板激活途径存在重大扰动。我们的蛋白质组学数据表明凝血途径蛋白（纤维蛋白原）升高，而许多补体蛋白减少。这些改变与诸如易患继发性细菌感染等功能后果相关，并可能导致局部和全身疾病表型。我们的数据提供了COVID-19病理学的新方面，其围绕COVID-19中脓毒症表型的存在。
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