Building on the framework of durable hematopoietic reprogramming, my current work investigates how chronic intestinal inflammation rewires the bone marrow compartment.
Using high-resolution single-cell multi-omic atlases of circulating HSPCs and their mature progeny in Crohn’s disease, I uncovered that inflammatory signals from the gut drive coordinated epigenetic and transcriptional changes across the hematopoietic hierarchy — from stem cells through committed progenitors to mature monocytes.
Using bone marrow chimera models, I demonstrated that colitis-primed progenitors autonomously amplify pathogenic inflammation, and that anti-TNF therapy can normalize these altered programs.