摘要：

Little is known about the immunologic aspects and the pathogenesis of the paranasal sinus mucocele.MethodsThe fluids of paranasal sinus mucoceles were obtained from 12 subjects. The concentration of macrophage migration inhibitory factor (MIF), interleukin 1β, tumor necrosis factor a, and regulated on activation normal T cell expressed and secreted (RANTES) were determined by enzyme-linked immunosorbent assay, and the levels of endotoxin were detected with kinetic Turbidimetric Assay.ResultsMIF and endotoxin were detected in the fluid of all samples, whereas interleukin-1β and RANTES were detected in 1 and 3 subjects out of 12 samples. Tumor necrosis factor a was not detected in any of the samples. A significant positive correlation between the levels of MIF and the period with symptoms such as pain, swelling of face, and visual disturbance was observed.ConclusionThese findings suggest that MIF and endotoxin may play an important role in the pathogenesis of paranasal sinus mucocele. MIF may be an important factor causing the development and exacerbation of the disease.ReferencesSection:1. Lund, V.J., and Milroy, C.M. Fronto-ethmoidal mucocoeles: A histopathological analysis. J Laryngol Otol 105: 921–923, 1991. Google Scholar2. Harvey, W., and Meghji, S. Prostaglandins in pathological bone resorption. Agents Actions 19: 73–79, 1986. Google Scholar3. Meghji, S. Bone remodelling. Br Dent J 172: 235–242, 1992. Google Scholar4. Meghji, S., Sandy, J.R., Scutt, A.M. Stimulation of bone resorption by lipoxygenase metabolites of arachidonic acid. Prostaglandins 36: 139–149, 1988. Google Scholar5. Lund, V.J., Harvey, W., Meghji, S. Prostaglandin synthesis in the pathogenesis of fronto-ethmoidal mucoceles. Acta Otolaryngol 106: 145–151, 1988. Google Scholar6. Lund, V.J., Henderson, B., and Song, Y. Involvement of cytokines and vascular adhesion receptors in the pathology of fronto-ethmoidal mucocoeles. Acta Otolaryngol 113: 540–546, 1993. Google Scholar7. Lorenzon, P., Vecile, E., Nardon, E. Endothelial cell E- and P-selectin and vascular cell adhesion molecule-1 function as signaling receptors. J Cell Biol 142: 1381–1391, 1998. Google Scholar8. David, J.R. Delayed hypersensitivity in vitro: Its mediation by cell-free substances formed by lymphoid cell-antigen interaction. Proc Natl Acad Sci USA 56: 72–77, 1966. Google Scholar9. Calandra, T., Bernhagen, J., Mitchell, R.A. The macrophage is an important and previously unrecognized source of macrophage migration inhibitory factor. J Exp Med 179: 1895–1902, 1994. Google Scholar10. Calandra, T., Bernhagen, J., Metz, C.N. MIF as a glucocorticoid-induced modulator of cytokine production. Nature 377: 68–71, 1995. Google Scholar11. Calandra, T., Echtenacher, B., LeRoy, D. Protection from septic shock by neutralization of macrophage migration inhibitory factor. Nat Med 6: 164–170, 2000. Google Scholar12. Kariya, S., Okano, M., Aoji, K. Role of macrophage migration inhibitory factor in otitis media with effusion in adults. Clin Diagn Lab Immunol 10: 417–422, 2003. Google Scholar13. Lai, K.N., Leung, J.C., Metz, C.N. Role for macrophage migration inhibitory factor in acute respiratory distress syndrome. J Pathol 199: 496–508, 2003. Google Scholar14. Metz, C.N., and Bucala, R. Role of macrophage migration inhibitory factor in the regulation of the immune response. Adv Immunol 66: 197–223, 1997. Google Scholar15. Butugan, O., Minoru Takeuti, M., Ganz Sanchez, T. Mucocele of the maxillary sinus. Rev Laryngol Otol Rhinol (Bord) 117: 11–13, 1996. Google Scholar16. Busaba, N.Y., and Kieff, D. Endoscopic sinus surgery for inflammatory maxillary sinus disease. Laryngoscope 112: 1378–1383, 2002. Google Scholar17. Lund, V.J. Anatomical considerations in the aetiology of fronto-ethmoidal mucoceles. Rhinology 25: 83–88, 1987. Google Scholar18. Harada, T., and Sakakura, Y. Immunologic responses against li-popolysaccharide of hemophilus influenzae in patients with acute sinusitis. Ann Otol Rhinol Laryngol 97: 207–210, 1988. Google Scholar, SAGE Journals19. Verduin, C.M., Hol, C., Fleer, A. Moraxella catarr

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