HUMAN NASAL EPITHELIUM ADSORBS COMPLEMENT C3-RELATED FRAGMENTS AND EXPRESSES CELL-MEMBRANE COMPLEMENT REGULATORY PROTEINS

Recent evidence suggests that complement is activated in human nasal a irways in inflammatory states, Activated complement protects the nasal mucosa against microorganisms, but also has the potential to lyse the host's normal cells, Complement-mediated cell lysis depends on adsorp tion of complement to the cell membrane and on uninterrupted activatio n of the complement cascade upon the same cell membrane, In the presen t study, the authors investigated first whether key complement compone nts, C3-related fragments, are adsorbed to nasal epithelial cell membr ane. Second, we investigated whether nasal epithelium expresses cell m embrane complement regulatory proteins that are known as interruptors tors of complement activation. Studies were done using fresh nasal muc osa obtained at turbinectomies from allergic rhinitis and vasomotor rh initis patients, In addition, in order to establish an in vitro model, studies were also done using primary cell cultures of nasal epitheliu m. We have found that complement CB-related fragments are present on c ell membranes of fresh nasal epithelium and that C3-related fragments are adsorbed to the epithelial cell membrane in nasal mucosa tissue se gments and in cell cultures that were incubated with autologous serum. Adsorption of C3-related fragments to the cell membrane of cultured n asal epithelial cells was found by flow cytometry analysis to be conce ntration-dependent. In addition, we found that nasal epithelium in fre sh tissue and in cell culture express three cell membrane complement r egulatory proteins: membrane cofactor protein (MCP, CD46), decay-accel erating factor (DAF, CD55), and CD59. Our findings in fresh nasal epit helium suggest that complement activation may occur upon the nasal epi thelial cell membrane during inflammation in vivo and that nasal epith elium might regulate this complement activation. Our in vitro cell cul ture model will allow further investigations of complement activation and regulation upon the human nasal epithelial cell membrane.