Functional and mechanistic study of the inhibitory role of the antisense long non-coding RNA (IRF1-AS1) in regulating the transcriptional activity of IRF1 and M1 polarization of macrophages in ARDS.

Through high-throughput sequencing and further cell and animal experiments, we found that the antisense long non-coding RNA of IRF1 (IRF1-AS1) binds to the intronic region of IRF1, inhibiting its transcriptional activity and thereby regulating macrophage activation and inflammation-induced lung injury in ARDS. CD14 cells were obtained from our hospital's biobank. After 48 hours of in vitro colony-stimulating factor induction, total RNA and DNA were extracted from cells treated with LPS and IFNγ for 24 hours. ChIP-seq/ATAC-seq and RNA-seq were performed using specific antibodies and assay kits.

本研究通过高通量测序结合后续细胞与动物实验，发现干扰素调节因子1（Interferon Regulatory Factor 1, IRF1）的反义长链非编码RNA（IRF1-AS1）可结合至IRF1的内含子区域，抑制其转录活性，进而调控急性呼吸窘迫综合征（Acute Respiratory Distress Syndrome, ARDS）中的巨噬细胞活化与炎症诱导性肺损伤。CD14细胞取自本院生物样本库。经体外集落刺激因子诱导48小时后，对经脂多糖（Lipopolysaccharide, LPS）与干扰素γ（Interferon γ, IFNγ）处理24小时的细胞提取总RNA与DNA，并使用特异性抗体与实验试剂盒开展染色质免疫沉淀测序（ChIP-seq）/转座酶可及性测序（ATAC-seq）及RNA测序（RNA-seq）实验。