Prerequisite for the process of breathing is a lubrication of pleural surfaces, provided by pleural mesothelium which is responsible for formation of pleural fluid. Information on a direct correlation of human pleural barrier function and molecular composition of the tight junction (TJ) however, is not available. Moreover, effects of pleural inflammation on barrier function have not been analyzed yet.

Methods: 

Transmesothelial resistance (R^tm) of healthy human visceral and parietal pleura specimens was analyzed in Ussing chamber experiments. TJ proteins were analyzed by Western blot and confocal laser scanning microscopy. Furthermore, inflamed human pleura specimens were analyzed.

Results: 

R^tm was 14.4 ± 1.9 W×cm² in visceral, and 17.9 ± 3.0 W×cm² in parietal pleura. Western blots detected occludin, claudin-1, -3, and -5, in both, visceral and parietal pleura, whereas claudin-7 was detected in visceral pleura only. A colocalization of occludin with claudins was detected by confocal laser scanning microscopy. Inflamed tissue specimens revealed a decrease of sealing tight junction proteins, and an induction of the paracellular cation and water channel claudin-2.

Conclusions: 

Human pleura shows expression of claudins known to be key determinants of epithelial barrier function, which is reflected by transmesothelial resistance. In addition, inflamed tissue specimens show a perturbed claudin expression which may directly account for a defective barrier function.