Endothelial Cells retain inflammatory memory through chromatin remodeling [ATAC-seq]
Sepsis survivors exhibit long-term endothelial dysfunction, increasing susceptibility to secondary infections such as pneumonia. To investigate the epigenetic and transcriptional basis of endothelial inflammatory memory, we employed transcriptomic profiling of primary endothelial cells exposed to inflammatory stimuli in a two-hit model. This study reveals persistent transcriptional reprogramming following IL-6 exposure and identifies a primed endothelial state that amplifies responses to secondary challenges. Overall design: Primary endothelial cells were treated with IL-6 or PBS for 72 hours (first hit), followed by a 48-hour washout phase. Nuclei were isolated for ATAC-seq from cells collected at two timepoints: immediately after the 72-hour treatment (IL6_72h, PBS_72h) and after the 48-hour washout (IL6_72h_W48h, PBS_72h_W48h). Each group included two or three biological replicates