Endothelial Cells retain inflammatory memory through chromatin remodeling [ATAC]

Sepsis survivors exhibit long-term endothelial dysfunction, increasing susceptibility to secondary infections such as pneumonia. To investigate the molecular basis of endothelial inflammatory memory, we performed transcriptomic profiling of lung and kidney endothelial cells isolated from a murine two-hit sepsis model. This model incorporates cecal ligation and puncture (CLP) as the primary inflammatory event, followed by a secondary intranasal challenge with Streptococcus pneumoniae. Overall design: Kidney endothelial cells isolated from mice subjected to a two-hit model of sepsis. The first hit involved cecal ligation and puncture (CLP) or sham surgery, followed by recovery. The second hit consisted of a secondary intranasal challenge with Streptococcus pneumoniae (SP) or PBS.