Daniel Gonsales Spíndola, Amber Bahr, Samantha Clark, Gabriel Pin de Jesus, Nina Martino, Anthony M. Lowery, Shuhan Lu, Andrew Seeman, Grace Martino, Giesse Albeche Duarte, Elijah Crosbourne, Peter Vincent, Guangchun Bai, Alejandro P. Adam, Katherine C. MacNamara, Ramon Bossardi Ramos
We uncover that endothelial cells retain a form of inflammatory memory, driven by chromatin remodeling and sustained JunB activity. Using two-hit models in mice and human endothelial cells, we show that an initial inflammatory exposure primes the endothelium for exaggerated responses to future inflammation. This discovery reveals a new mechanism of chronic endothelial dysfunction and identifies JunB as a potential therapeutic target in postsepsis care.