BACKGROUND: Immunosuppression is the leading cause of recurrent sinus infections after hematopoietic stem cell transplant (HSCT), with increased incidence of sinusitis in patients with chronic graft versus host disease (GVHD). Histological descriptions of the oral mucosa, lung ciliary epithelium, and intestinal mucosa related to HSCT have been described. However, few have described the nasal mucosa. We, therefore, sought to elucidate the histological and ultrastructural features of the nasal mucosa in patients after HSCT to better understand the pathophysiology of the immune response. METHODS: Uncinate processes from 24 HSCT patients and 12 immunocompetent patients were subjected to histological analyses via light and transmission electron microscopy (TEM). RESULTS: TEM revealed aberrant cilia structure, altered mitochondria quantity, microvilli, and cytoplasm vacuolization. All HSCT patients with rhinosinusitis had significant loss or absence of cilia (p = 0.018). Apoptotic bodies were increased and Goblet cells decreased in nasal epithelium from patients with chronic GVHD (p = 0.04). CONCLUSION: This tissue destruction likely enhances pathogen penetration resulting in recurrent infection.
BACKGROUND: Immunosuppression is the leading cause of recurrent sinus infections after hematopoietic stem cell transplant (HSCT), with increased incidence of sinusitis in patients with chronic graft versus host disease (GVHD). Histological descriptions of the oral mucosa, lung ciliary epithelium, and intestinal mucosa related to HSCT have been described. However, few have described the nasal mucosa. We, therefore, sought to elucidate the histological and ultrastructural features of the nasal mucosa in patients after HSCT to better understand the pathophysiology of the immune response. METHODS: Uncinate processes from 24 HSCT patients and 12 immunocompetent patients were subjected to histological analyses via light and transmission electron microscopy (TEM). RESULTS: TEM revealed aberrant cilia structure, altered mitochondria quantity, microvilli, and cytoplasm vacuolization. All HSCT patients with rhinosinusitis had significant loss or absence of cilia (p = 0.018). Apoptotic bodies were increased and Goblet cells decreased in nasal epithelium from patients with chronic GVHD (p = 0.04). CONCLUSION: This tissue destruction likely enhances pathogen penetration resulting in recurrent infection.