The CCR2 inflammatory pathway is a target for improving severe disease and pulmonary inflammation in experimental COVID-19_Raw data

In this study, we used the K18-hACE2 mouse model of SARS-CoV-2 Delta variant infection to investigate the role of the CCR2 inflammatory pathway in COVID-19 pathogenesis. The data included here shows that CCR2 ligands (CCL2/7/8) were among the most upregulated transcripts in infected lungs, and that therapeutic blockade of CCR2 signaling significantly improved clinical outcomes, reduced pulmonary inflammation, and modulated cytokine responses. These findings highlight CCR2 as a promising immunomodulatory target for treating viral-induced acute respiratory distress syndrome (ARDS).本研究采用新型冠状病毒德尔塔变异株（SARS-CoV-2 Delta variant）感染的K18-hACE2小鼠模型（K18-hACE2 mouse model），探究CCR2炎症通路在新型冠状病毒肺炎（COVID-19）致病机制中的作用。本研究所收录的数据显示，感染小鼠肺部中上调幅度最高的转录本包含CCR2配体（CCL2/7/8）；通过治疗性阻断CCR2信号通路，可显著改善临床结局、减轻肺部炎症并调控细胞因子应答。上述研究结果表明，CCR2可作为治疗病毒诱导型急性呼吸窘迫综合征（ARDS）的极具前景的免疫调节靶点。