Expression of CC16 in the lung tissues of rats with acute lung injury and its modulation on the local inflammatory reactions in lungs

To investigate the role of CC16 on the pathogenesis of acute lung injury(ALI) induced by lipopolysaccharide (LPS), 56 male Sprague-Dawley(SD) rats were randomly divided into control group and the 6 experimental groups, while in the experimental groups, ALI were induced by LPS at 0.5, 1, 2, 4, 6 and 24 hours respectively. The pulmonary alveolar septa area density (PASAD) and the numbers of polymorphonuclear leukocytes (PMN) and the contents of CC16 and pro-inflammatory cytokines TNF and IL-6 in rat lung tissues were analyzed morphometrically, and were assayed by Western blotting and immunoradioassay respectively. Semi-quantitative RT-PCR was used to detect the expression level of CC16 mRNA, and immunofluorescence and Western blotting were carried out to assess the expression and activation of NF-кB in rat lung tissues. The experimental results showed that the PASAD and numbers of PMN in the lung tissues of rats with ALI were significantly increased at 0.5 hours post-injury by LPS and both peaked after 6 hours of injury, but returned to values of baseline at 24 hours. The contents of CC16 in the lung tissues of rats with ALI at 0.5, 1, 2, 4, 6 and 24 hours were (0.74±0.212), (0.630±0.148), (0.603±0.111), (0.570±0.125), (0.529±0.124) and (0.614±0.185) respectively, that was significantly lower than that of the control group. Also, the levels of the CC16 mRNA in the lung tissues of ALI rats at different times were significantly lower than that the control group. Meanwhile, the numbers of the NF-κB-positive cells of ALI rats at different times were larger than that of the control group, but the contents of IκB-α at different times of the ALI rats were significantly lower than that of the control groups. In addition, the level of TNF in the lung homogenates showed an immediate elevation after LPS injection, attained to a higher level than that of the control group after 0.5 hours, reached to its peak value at one hour, maintained to high level until 6 hours and then gradually recovered. While, the level of IL-6 in the lung homogenates of ALI rats began to rise an hour post- mjury, peaked at 4 hours and then gradually returned to normal level after 6 hours. It is evident that CC16 correlates significantly with all the indices mentioned above, suggesting that it could modulate the local inflammatory reactions in lungs and may play a critical role in the pathogenesis of acute lung injuries induced by LPS.