Abstract

Although the mechanisms controlling the resolution of inflammatory processes are still not clear, it is thought that a number of inflammatory cells, including neutrophils and eosinophils, and ingestion of these cells by macrophages may be involved in the apoptotic cell process in allergic or non-allergic nasal tissues. We postulated that apoptosis of inflammatory cells may occur in vivo in nasal mucosa, thus regulating allergic and non-allergic inflammation, and to test this hypothesis we examined apoptotic cells in the nasal tissue of surgical specimens. Human turbinates were obtained after conchotomy performed on patients with nasal obstruction refractory to medication. Nasal tissues were fixed in formalin and embedded in paraffin. The paraffin-embedded tissues were stained for apoptotic cells by terminal deoxynucleotidyl transferase-mediated deoxyuridine 5′-triphosphate (dUTP) nick end-labeling (TUNEL). To identify cell types undergoing apoptosis, double staining was performed by combining TUNEL and immunohistochemistry. The majority of TUNEL-positive cells were identified as leukocytes. Most TUNEL-positive cells found in these tissues represented granulocytes. A higher proportion of TUNEL-positive cells was found to be macrophages and most TUNEL-positive macrophages had intact nuclei and contained phagocytosed TUNEL-positive material (assumed to be apoptotic cells or bodies) in the cytoplasm. These experiments represent the demonstration of cell type-specific apoptosis in human nasal mucosa. The results may have an important clinical implication and also promote further investigation to control the apoptosis of these cells in health and disease.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.