Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the ensuing COVID-19 pandemic have caused ∼40 million cases and over 648,000 deaths in the United States alone. Troubling disparities in COVID-19-associated mortality emerged early, with nearly 70% of deaths confined to Black/African-American (AA) patients in some areas, yet targeted studies within this demographic are scant. Multi-omics single-cell analyses of immune profiles from airways and matching blood samples of Black/AA patients revealed low viral load, yet pronounced and persistent pulmonary neutrophilia with advanced features of cytokine release syndrome and acute respiratory distress syndrome (ARDS), including exacerbated production of IL-8, IL-1β, IL-6, and CCL3/4 along with elevated levels of neutrophil elastase and myeloperoxidase. Circulating S100A12⁺/IFITM2⁺ mature neutrophils are recruited via the IL-8/CXCR2 axis, which emerges as a potential therapeutic target to reduce pathogenic neutrophilia and constrain ARDS in severe COVID-19.

中文翻译：

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致病性中性粒细胞增多导致重症 COVID-19 患者出现急性呼吸窘迫综合征

仅在美国，严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 和随之而来的 COVID-19 大流行就造成了约 4000 万例病例和 648,000 多例死亡。COVID-19 相关死亡率的令人不安的差异很早就出现了，在某些地区，近 70% 的死亡仅限于黑人/非裔美国人 (AA) 患者，但在这一人群中的针对性研究很少。对来自气道的免疫谱和黑人/AA 患者的匹配血液样本的多组学单细胞分析显示病毒载量低，但肺中性粒细胞明显且持续存在，具有细胞因子释放综合征和急性呼吸窘迫综合征 (ARDS) 的高级特征，包括加重IL-8、IL-1β、IL-6 和 CCL3/4 的产生以及中性粒细胞弹性蛋白酶和髓过氧化物酶水平升高。循环S100A12⁺ /IFITM2 ⁺成熟中性粒细胞通过 IL-8/CXCR2 轴被招募，这成为减少致病性中性粒细胞增多症和限制严重 COVID-19 中 ARDS 的潜在治疗靶点。