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Title: In vitro studies of the bronchial epitheluim in COPD.
Author: Sanleng, S.
ISNI:       0000 0001 3551 5520
Awarding Body: Queens University Belfast
Current Institution: Queen's University Belfast
Date of Award: 2008
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Background: The bronchial epithelium (BE) performs many diverse functions to protect the respiratory tract from inhaled particles and pathogens. Alterations of this tissue are implicated in the pathophysiology of chronic obstructive pulmonary disease (COPD). COPD is a characterized by progressive and irreversible airflow limitation and is cunently the fourth-leading cause of death worldwide. Cigarette smoking (CS) is the major risk factor for its development. The presellt study examined several aspects of BE ill vitro with the final aims of investigating the effect of CS on its innate immunity function, the irreversibility of its phenotypic and functional alterations in COPD and its cellular interaction with macrophages which are also implicated in COPD. Materials and Methods: Bronchial epithelial cell (BEC) lines and primary BEC isolated from COPD and Control subjects were used. Primary BEC were differentiated at the air-liquid interface to create a cellular model that resembles the structure and function of BE ill vivo. BEC were also co-cultured with THP-l monocytic cell line to mimic interaction with macrophages. Results: CS modulated the bacterial and viral induced-innate immune responses from BEC and altered the intracytoplasmic expression of specific toll-like receptors leading to an increased susceptibility to infections. By comparing Control and COPD well-differentiated BEC, it was shown that several important alterations of the COPD BE are irreversible. Moreover, BEC and macrophages interacted with each other to modify their inflammatory responses emphasising the importance of this cell-cell communication in COPD. Conclusions: Smoking cessation appears critical in the prevention of infection and the management of COPD. Future therapies for COPD should focus on the irreversible alterations described in this study to prevent fmther deteriorations in patients with COPD. Finally, it appe~rs fundamental that future researches are performed in cellular models that mimic the ill vivo structure and cell-cell interactions of the airways.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available