新冠肺炎患者和细菌性肺炎患者血清差异表达的细胞因子特征分析

Longitudinal characteristics of cytokine profiles in the peripheral blood of COVID-19 and bacterial pneumonia patients

目的了解新型冠状病毒肺炎(新冠肺炎)患者与细菌性肺炎患者细胞因子的差异,探讨新冠肺炎免疫病理机制,为新冠肺炎提供新的治疗靶点。方法收集轻型新冠肺炎患者(新冠肺炎组)、细菌性肺炎患者(细菌性肺炎组)和健康志愿者(健康对照组)3组各15份血清标本,进行48种细胞因子的检测,比较3组间细胞因子表达谱的差异。检测10例新冠肺炎患者在治疗不同时间点的血清标本中48种细胞因子表达,分析其与新冠肺炎患者的临床特征及疾病进展的相关性。结果新冠肺炎组与细菌性肺炎组比较中,巨噬细胞迁移抑制因子(MIF)、生长调节致癌基因α(GROα)、粒细胞-巨噬细胞集落刺激因子(GM-CSF)和TNF-β在新冠肺炎组中上调(P均<0.05)。而IL-10、IL-18、IL-2受体α和IFN-γ诱导的单核细胞因子(MIG)在细菌性肺炎组中上调(P均<0.05)。巨噬细胞集落刺激因子(M-CSF)在新冠肺炎患者住院治疗的第2周有明显的下调;单核趋化蛋白-1(MCP-1)的变化与新冠肺炎患者的核酸检测结果变化一致。结论新冠肺炎患者和细菌性肺炎患者体内存在不同的细胞因子表达谱。M-CSF和MCP-1在新冠肺炎疾病进展中起着重要作用。

Objective To investigate the differences of cytokine profiles between patients with novel COVID-19 and bacterial pneumonia,unravel the immunopathological mechanism of COVID-19,and provide evidence for new therapeutic targets in COVID-19.Methods In this study,15 serum samples were collected from mild COVID-19 patients(COVID-19 group),bacterial pneumonia patients(bacterial pneumonia group),and healthy controls(healthy control group),respectively.The expression profile of 48 cytokines was determined to clarify the differences among three groups.The expression levels of 48 cytokines at different time points were measured in serum samples from 10 patients with COVID-19 to analyze their correlation with clinical features and disease progression.Results In the comparation between the COVID-19 group and the bacterial pneumonia group,the expression levels of MIF,GROα,GM-CSF and TNF-βwere upregulated in COVID-19 patients(all P<0.05),whereas those of IL-10,IL-18,IL-2Rαand MIG were upregulated in patients with bacterial pneumonia(all P<0.05).The expression level of M-CSF was significantly downregulated in COVID-19 patients at the second week of hospitalization.The changes in the expression level of MCP-1 were consistent with the nucleic acid test results of COVID-19 patients.Conclusions The cytokine profiles differ between patients with COVID-19 and bacterial pneumonia.In addition,M-CSF and MCP-1 play critical roles in the progression of COVID-19.