Endothelial Cells retain inflammatory memory through chromatin remodeling II

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 performed transcriptomic profiling of primary human endothelial cells exposed to sequential inflammatory stimuli in a two-hit in vitro model. IL-6 priming induced sustained transcriptional reprogramming and heightened responsiveness to a secondary LPS challenge, indicative of a memory-like state. To mechanistically dissect this response, we silenced the AP-1 transcription factor JunB using siRNA during the priming phase and evaluated its role in shaping the inflammatory memory response. These studies provide insight into the molecular circuitry maintaining endothelial memory and identify JunB as a potential regulator of this process.