Endothelial Cells retain inflammatory memory through chromatin remodeling [RNA-Seq 2]
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: RNA was extracted from lung and 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. Endothelial cells were isolated at defined time points and RNA-seq was performed using the Illumina NovaSeq 6000 platform (paired-end). A total of 54 samples representing various treatment groups across lung and kidney tissues were analyzed to identify gene expression signatures associated with endothelial inflammatory memory.