IADR Abstract Archives
Goblet cell mucin and the pathogenesis of salivary gland ductal stricture
Objectives: The aim of the study was to investigate whether ductal cells in the affected gland undergo transdifferentiation into metaplastic and hyperplastic cells which may eventually leads to stricture formation
Methods: Mucoid plugs were collected from the Stenson’s duct of the affected gland of patients and analyzed for the presence of mucins. An in-vivo experiment was conducted which involved the introduction of the bacterial mimic lipopolysaccharide (LPS) into the parotid duct followed by assessment of metaplastic and hyperplastic changes by the ductal cells.LPS induced signaling was examined in a human parotid duct (HSY) cell line. Real time PCR and western blots were performed to demonstrate if thier is an increased expression of TLR4 on ductal epithelial cells in response to bacteria (LPS).
Results: The parotid gland does not secrete mucin yet stricture formation is associated with the presence of ‘mucoid plugs’. We collected mucoids plugs from patients with stricture and identified the presence of mucins (MUC5AC, MUC5B, MUC2, and MUC1) using SDSPAGE/ proteomics analysis and western blotting. Thus, under pathological conditions the parotid gland expresses aggregates (mucoid plugs) containing mucin and proteins associated with defense and inflammation.
An in-vivo experimental model was developed in which lipopolysaccharide (LPS) was instilled into the parotid ducts of rats. After 7 days tissue was removed, fixed and examined morphologically. Inflammatory cell infiltrates in the main parotid duct were associated with increased expression of TLR4 and the novel appearance of MUC5AC containing goblet cells in the ductal epithelium.
LPS induced signaling was examined in a human parotid duct (HSY) cell line. Real time PCR and western blots results demonstrated an increased expression of TLR4 on ductal epithelial cells in response to bacteria (LPS).
Conclusions: In conclusion, it appears that goblet cell metaplasia and aberrant mucin production occurs in the main duct of the parotid gland in response to infection. The formation of plugs of mucous in the duct and persistence of infection may be a causative factor in stricture and obstructive disease.
Methods: Mucoid plugs were collected from the Stenson’s duct of the affected gland of patients and analyzed for the presence of mucins. An in-vivo experiment was conducted which involved the introduction of the bacterial mimic lipopolysaccharide (LPS) into the parotid duct followed by assessment of metaplastic and hyperplastic changes by the ductal cells.LPS induced signaling was examined in a human parotid duct (HSY) cell line. Real time PCR and western blots were performed to demonstrate if thier is an increased expression of TLR4 on ductal epithelial cells in response to bacteria (LPS).
Results: The parotid gland does not secrete mucin yet stricture formation is associated with the presence of ‘mucoid plugs’. We collected mucoids plugs from patients with stricture and identified the presence of mucins (MUC5AC, MUC5B, MUC2, and MUC1) using SDSPAGE/ proteomics analysis and western blotting. Thus, under pathological conditions the parotid gland expresses aggregates (mucoid plugs) containing mucin and proteins associated with defense and inflammation.
An in-vivo experimental model was developed in which lipopolysaccharide (LPS) was instilled into the parotid ducts of rats. After 7 days tissue was removed, fixed and examined morphologically. Inflammatory cell infiltrates in the main parotid duct were associated with increased expression of TLR4 and the novel appearance of MUC5AC containing goblet cells in the ductal epithelium.
LPS induced signaling was examined in a human parotid duct (HSY) cell line. Real time PCR and western blots results demonstrated an increased expression of TLR4 on ductal epithelial cells in response to bacteria (LPS).
Conclusions: In conclusion, it appears that goblet cell metaplasia and aberrant mucin production occurs in the main duct of the parotid gland in response to infection. The formation of plugs of mucous in the duct and persistence of infection may be a causative factor in stricture and obstructive disease.