Inflammatory memory primes the intestine for enhanced regenerative potential [ATAC-seq]

To investigate whether IFNγ signaling plays an instructive role in driving long-term epigenetic reprogramming after injury, we performed bulk ATAC-seq on epithelial cells isolated from mice under three conditions: unirradiated controls, irradiated mice 21 days post-injury, and irradiated mice treated with anti-IFNγ blocking antibody during the recovery phase.

This approach allowed us to assess how IFNγ inhibition influences chromatin accessibility and the establishment of inflammatory memory in intestinal epithelial cells following radiation injury.