Files
Abstract
Tissue regeneration requires carefully balanced cell proliferation, and our previous work shows that fusion between bone marrow–derived cells (BMDCs) and intestinal epithelial cells occurs after injury as a potential repair mechanism. This thesis investigates the environmental cues and cell types that drive intestinal cell fusion and examines the properties of resulting fusion hybrids. Using transplantation and parabiosis models, I identify local inflammation and epithelial hyperproliferation as key mediators of fusion. Donor immune cells—primarily macrophages—cluster around injured crypts before fusion occurs. Transcriptome analysis reveals that fusion hybrids retain both epithelial and macrophage signatures. These findings demonstrate that cell fusion generates unique hybrid cells with potential roles in regeneration and tumorigenesis and suggest a mechanistic link between intestinal inflammation and cancer.