Source: International Congress 2014 – COPD: points to ponder
Disease area: Airway diseases

Abstract

Background: MUC5AC and MUC5B are major mucin subtypes in the lung epithelium. Bronchial epithelial MUC5AC expression is increased in COPD patients compared to controls, while no difference has been found for MUC5B. We have investigated MUC5B expression in COPD patients with persistent sputum production, as previous studies may not have included patients with severe chronic bronchitis. We have also studied the expression of HIF-1a; this transcription factor accumulates rapidly during hypoxia and may regulate mucin expression.Methods: The distribution of MUC5AC, MUC5B, HIF-1a and its downstream marker CAIX in the bronchial epithelium of COPD persistent sputum producers, COPD patients without sputum production and healthy controls were analyzed by immunohistochemistry. Dimethyloxalylglycine (DMOG) was used to upregulate HIF-1a expression in bronchial epithelial cells, and subsequent changes in MUC5B expression were evaluated.Results: MUC5B and CAIX expression in the bronchial epithelium was significantly higher in COPD persistent sputum producers compared to COPD sputum non-producers (p = 0.04 and p = 0.002), and healthy controls. MUC5AC expression was similar in COPD persistent sputum producers compared to non-producers, with higher expression in both COPD groups compared to healthy controls. CAIX expression correlated to HIF-1a expression (r = 0.85, p < 0.0001). DMOG increases HIF-1a and MUC5B expression.Conclusion: COPD persistent sputum producers have increased MUC5B and CAIX expression in the bronchial epithelium. HIF-1a can potentially increase MUC5B expression, implicating this hypoxia inducible transcription factor in mucus hypersecretion in COPD.

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Citations should be made in the following way:
S. Khurana, K. Brown, J. Vestbo, J. Plumb, D. Singh (Manchester, United Kingdom). Increased MUC5B and carbonic anhydrase IX expression in the bronchial epithelium of COPD persistent sputum producers. Eur Respir J 2014; 44: Suppl. 58, 3626

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