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Volume 97, Issue 1, Pages 59-64 (January 2003)


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Down-regulation of aquaporin 3 in bronchiectatic airways in vivo

K.W TSANGa, J.C LEUNGa, G.L TIPOEb, R LEUNGa, C YANa, G.C OOIc, H.H CHANa, W.K LAMa, K.N LAIaf1

Received 22 January 2002; accepted 27 May 2002.

Abstract 

Bronchiectasis is characterized pathologically by permanent abnormal bronchial dilation, and clinically by chronic sputum production. Aquaporin 3 (AQP3), a recently described water channel that is also found in large airway cell membrane, could play a role in the pathogenesis and particularly that of bronchorrhea in bronchiectasis. However, little is known of its in vivo distribution and physiological role in human airways. We have, therefore, performed this quantitative immunohistochemistry study on endobronchial biopsies to evaluate the expression and clinical relevance of AQP3 in patients with idiopathic bronchiectasis (n=25, 15 F, 64.3±11.5 years) and control subjects (n=14, 5 F, 57.5±12.0 years). Quantitative image analysis was performed to evaluate the expression of AQP3 in the bronchial epithelial cells. Our results show that AQP3 was predominantly expressed in the basal cells of the epithelial layer in both groups. Expression of AQP3 was significantly reduced in the basal, but not columnar, epithelial cells in bronchiectasis compared with control airways (p=0.02, 0.35). Only bronchiectatic patients with regular sputum production, but not their counterparts, had significant downregulation of epithelial AQP3 expression compared with control airways (p=0.004, 0.24). Our findings suggest that AQP3 could have an important role in the pathogenesis of increased mucus production in bronchiectasis.

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a University Department of Medicine

b University Department of Anatomy

c University Department of Diagnostic Radiology, The University of Hong Kong, Hong Kong, SAR, China

f1 Correspondence should be addressed to: Prof Kar N Lai, DSc, MD, FRCP, FRCPath, University Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Pokfulam Road, Hong Kong SAR, China. Fax: +852 28162863; E-mail: knlai@hkucc.hku.hk

PII: S0954-6111(02)91413-7

doi:10.1053/rmed.2002.1413


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