In our nose, the sense of smell is mediated by the olfactory mucosa, a neuroepithelial tissue containing long-lived olfactory stem cells. Even though these stem cells possess a remarkable capacity for regeneration, the loss of the sense of smell is a common symptom in the setting of chronic inflammatory rhinosinusitis. Deepening our understanding of the stem cell behavior has the potential to inform novel treatment strategies for inflammation-related olfactory deficits.
In Andrew Lane’s Lab, my research focuses on the cross-talk between olfactory stem cells and the local immune system in acute or chronic inflammation. We observed that the basal stem cell population was activated in the inflammatory environment and directly contributed to the disease pathology. Our study establishes a mechanism of chronic rhinosinusitis-associated olfactory loss, caused by a functional switch of neuroepithelial stem cells from regeneration to immune defense. The immune activity of basal stem cells in communicating with infiltrating inflammatory cells may play a more generalized role in mucosal immunity at epithelial barrier surfaces in health and disease.