Mitochondrial N-formyl methionine peptides contribute to exaggerated neutrophil activation in patients with COVID-19.
Mitochondrial N-formyl methionine peptides contribute to exaggerated neutrophil activation in patients with COVID-19.
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DOI：
10.1080/21505594.2023.2218077
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发表时间：
2023-12
期刊：
影响因子：
5.2
通讯作者：
Lood, Christian
中科院分区：
文献类型：
--
作者：
Kuley, Runa;Duvvuri, Bhargavi;Wallin, Jeffrey J.;Bui, Nam;Adona, Mary Vic;O'Connor, Nicholas G.;Sahi, Sharon K.;Stanaway, Ian B.;Wurfel, Mark M.;Morrell, Eric D.;Liles, W. Conrad;Bhatraju, Pavan K.;Lood, Christian
关键词：
神经元失调在COVID-19中得到了很好的证实。然而，导致COVID-19中性粒细胞活化的因素尚不清楚。我们评估了N-甲酰甲硫氨酸（fMet）是否有助于COVID-19中的中性粒细胞活化。与HC相比，在COVID-19患者（n = 68）中观察到钙卫蛋白、中性粒细胞胞外陷阱（NET）和fMet水平升高，特别是在重症患者中（n = 19，p < 0.0001）。值得注意的是，患有COVID-19的ICU患者的NET水平高于没有COVID-19的ICU患者（p < 0.05），表明NET在COVID-19中的突出贡献。此外，来自具有轻度和中度/重度症状的COVID-19患者的血浆通过fMet/FPR 1（甲酰肽受体-1）依赖性机制诱导体外中性粒细胞活化（p < 0.0001）。fMet水平与钙卫蛋白水平相关，验证了COVID-19患者中fMet介导的中性粒细胞活化（r = 0.60，p = 0.0007）。我们的数据表明，fMet是导致COVID-19疾病中性粒细胞活化的重要因素，可能是治疗干预的潜在靶点。
Neutrophil dysregulation is well established in COVID-19. However, factors contributing to neutrophil activation in COVID-19 are not clear. We assessed if N-formyl methionine (fMet) contributes to neutrophil activation in COVID-19. Elevated levels of calprotectin, neutrophil extracellular traps (NETs) and fMet were observed in COVID-19 patients (n = 68), particularly in critically ill patients, as compared to HC (n = 19, p < 0.0001). Of note, the levels of NETs were higher in ICU patients with COVID-19 than in ICU patients without COVID-19 (p < 0.05), suggesting a prominent contribution of NETs in COVID-19. Additionally, plasma from COVID-19 patients with mild and moderate/severe symptoms induced in vitro neutrophil activation through fMet/FPR1 (formyl peptide receptor-1) dependent mechanisms (p < 0.0001). fMet levels correlated with calprotectin levels validating fMet-mediated neutrophil activation in COVID-19 patients (r = 0.60, p = 0.0007). Our data indicate that fMet is an important factor contributing to neutrophil activation in COVID-19 disease and may represent a potential target for therapeutic intervention.
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