Expression of Trefoil factor family peptides in the nasal allergic mucosa.

OBJECTIVE: Trefoil factor family peptides (TFFs) are the secretory products of mucous cells and are closely associated with mucins. TFFs appear to be important in mucosal healing processes. Although TFF1/3 are expressed in the human respiratory tract, their role in the nasal mucosa is not thoroughly understood. We investigated the association between TFFs and mucins and the role TFFs in the human nasal mucosa. MATERIAL AND METHODS: Patients undergoing turbinectomy were included and it was determined whether patients had nasal allergies or not. The localization of TFF1/3, MUC5AC/5B expression was investigated using immunohistochemistry. The levels of the mRNA transcripts were examined using quantitative real-time PCR. RESULTS: TFF1/3 had a similar pattern of localization in epithelial goblet cells and submucosal glandular cells. TFF1/3 co-localized with MUC5AC in the epithelium, and co-localized with MUC5B in the epithelium and the submucosal glandular cells. The levels of TFF1/3 and MUC5B mRNA in allergic patients were significantly increased. CONCLUSION: Our results suggest that TFF1/3 may associate with MUC5AC and MUC5B in the nasal mucosa, and that up-regulation of TFF1/3 and MUC5B may play an important role in the clinical condition of the nasal allergic mucosa.

Analysis of syndecan-1 and TGF-beta expression in the nasal mucosa and nasal polyps.

OBJECTIVE: Increased understanding of cytokines and their associated proteoglycans will contribute to the investigation of the formation of nasal polyps. Recently, some studies have suggested that syndecan-1 ectodomains are shed in response to low respiratory infection, but no studies regarding nasal and paranasal diseases have been reported. Transforming growth factor-beta (TGF-beta) is involved in the regulation of nasal polyps, especially in processes crucial to the initiation, maintenance, and resolution of inflammatory responses. In the nasal mucosa and nasal polyps, we analyzed the expression of syndecan-1, which readily promotes infection, and TGF-beta, which plays a role in syndecan-1 activity. METHODS: Fifteen patients who underwent turbinectomy for the treatment of nasal obstruction and seventeen patients with nasal polyps who underwent nasal endoscopic sinus surgery were included in this study. The localization of syndecan-1 and TGF-beta in the nasal mucosa and nasal polyps was investigated by immunohistochemistry, and mRNA transcript levels of syndecan-1 and TGF-beta were examined using quantitative real-time PCR. RESULTS: Immunohistochemical staining revealed that the expression of syndecan-1 in the nasal mucosa and nasal polyps was co-localized with TGF-beta. The mean mRNA expression values for syndecan-1 and TGF-beta were higher in nasal polyps compared to the nasal mucosa. CONCLUSIONS: This is the first report showing expression of syndecan-1 in the nasal mucosa and nasal polyps. In nasal polyps, syndecan-1 expression may be increased by an unknown mechanism, permitting infection and inducing larger nasal polyps. We hypothesize that the accumulation of TGF-beta, which is involved in the pathophysiological development of nasal polyps, may result in a change in the binding properties of syndecan-1 at inflammatory sites.