Ultrastructural changes in platelet activating factor-induced epithelial damage in rabbit maxillary sinus mucosa

Citation
Sy. Jeon et al., Ultrastructural changes in platelet activating factor-induced epithelial damage in rabbit maxillary sinus mucosa, ANN OTOL RH, 109(8), 2000, pp. 726-730
Citations number
16
Categorie Soggetti
Otolaryngology,"da verificare
Journal title
ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY
ISSN journal
00034894 → ACNP
Volume
109
Issue
8
Year of publication
2000
Part
1
Pages
726 - 730
Database
ISI
SICI code
0003-4894(200008)109:8<726:UCIPAF>2.0.ZU;2-9
Abstract
Platelet activating factor (PAF), a potent chemical mediator in inflammatio n and allergic reaction, has been thought to induce mucociliary inhibition and epithelial damage in the airway mucosa. However, several recent papers have reported that PAF may not readily damage the airway epithelium. The ai m of this study was to elucidate the pathogenesis of PAF-induced epithelial damage in terms of ultrastructural changes. Sixteen micrograms of PAF (1 m L of 16 mu g/mL) wets administered into the maxillary sinuses of rabbits, T he rabbits were divided into groups according to time intervals, and the an tral mucosa was taken 1 and 3 days after administration of PAF. The tissue was processed for routine transmission electron microscopy. No epithelial d egeneration was observed other than platelet aggregation, red blood cell st asis, and swelling of the endothelial cells 1 day after administration of P AF. Migration of inflammatory cells into the perivascular connective tissue , infiltration of eosinophils into the subepithelial and intraepithelial sp aces, and vacuolar degeneration of the epithelial cells with focal loss of cilia were seen 3 days after administration of PAF. In conclusion, PAF indu ced infiltration of eosinophils into the epithelium, and resulted ill epith elial degeneration that varied according to the time interval. Our findings suggest that PAF may cause epithelial damage through a series of secondary events, probably due to cytotoxicity of eosinophils infiltrating the epith elium.