OBJECTIVES: To examine changes in aquaporin 1 (AQP1) and aquaporin 5 (AQP5) in the small airways and alveoli in a rat asthma model. METHOD: Forty Wistar rats were randomly divided into a control group and an ovalbumin (OVA) sensitization asthma model group. The distribution and expression of AQP1 and AQP5 in lung tissues were analyzed using immunohistochemistry (IHC), quantified the staining intensity by assessing integrated optical densities (IOD), and Western blotting (WB). RESULTS: IHC showed AQP1 was mainly distributed in sub-epithelial microvascular endothelial cells (MECs) and red blood cells. IOD values showed, in the asthma model group, the expression of AQP1 in alveolar MECs was lower than that in the control group (P<0.05); However, AQP1 expression in small airways sub-epithelial was higher than in the control group (P<0.05). The WB indicated that AQP1 expression in the asthma model group was 57% lower than in the control group (P<0.05). AQP5 was mainly distributed in the non-ciliated epithelial cells of the small airways and the apical membranes of type I and type II epithelial cells. IOD values showed, in asthma model group, the expression of AQP5 increased in small airways epithelium (P<0.05), and decreased in alveolar epithelium (P<0.05). The WB showed a 36% reduction in AQP5 expression compared with the control group (P<0.05). CONCLUSION: AQP1 and AQP5 increased in small airways in rats with experimentally induced asthma, indicating that they may be involved in the formation of submucosal edema and mucus hypersecretion. Decreased AQP1 and AQP5 in pulmonary alveoli may be related to increased alveolar liquid viscosity and the formation of mucus plugs.
OBJECTIVES: To examine changes in aquaporin 1 (AQP1) and aquaporin 5 (AQP5) in the small airways and alveoli in a ratasthma model. METHOD: Forty Wistar rats were randomly divided into a control group and an ovalbumin (OVA) sensitization asthma model group. The distribution and expression of AQP1 and AQP5 in lung tissues were analyzed using immunohistochemistry (IHC), quantified the staining intensity by assessing integrated optical densities (IOD), and Western blotting (WB). RESULTS: IHC showed AQP1 was mainly distributed in sub-epithelial microvascular endothelial cells (MECs) and red blood cells. IOD values showed, in the asthma model group, the expression of AQP1 in alveolar MECs was lower than that in the control group (P<0.05); However, AQP1 expression in small airways sub-epithelial was higher than in the control group (P<0.05). The WB indicated that AQP1 expression in the asthma model group was 57% lower than in the control group (P<0.05). AQP5 was mainly distributed in the non-ciliated epithelial cells of the small airways and the apical membranes of type I and type II epithelial cells. IOD values showed, in asthma model group, the expression of AQP5 increased in small airways epithelium (P<0.05), and decreased in alveolar epithelium (P<0.05). The WB showed a 36% reduction in AQP5 expression compared with the control group (P<0.05). CONCLUSION:AQP1 and AQP5 increased in small airways in rats with experimentally induced asthma, indicating that they may be involved in the formation of submucosal edema and mucus hypersecretion. Decreased AQP1 and AQP5 in pulmonary alveoli may be related to increased alveolar liquid viscosity and the formation of mucus plugs.
Authors: Kieran Brune; James Frank; Andreas Schwingshackl; James Finigan; Venkataramana K Sidhaye Journal: Am J Physiol Lung Cell Mol Physiol Date: 2015-01-30 Impact factor: 5.464