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Mediators of Inflammation
Volume 2013, Article ID 159349, 13 pages
Research Article

TNF- Regulates Natriuretic Peptides and Aquaporins in Human Bronchial Epithelial Cells BEAS-2B

1Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Polo Unico Sant’Andrea delle Fratte, 06156 Perugia, Italy
2Thoracic Surgery Unit, Ospedale S. Maria della Misericordia, University of Perugia, S. Andrea delle Fratte, 06156 Perugia, Italy
3Clinical Pathology and Hematology Unit, Ospedale S. Maria della Misericordia of Perugia, S. Andrea delle Fratte, 06156 Perugia, Italy

Received 15 May 2013; Revised 26 August 2013; Accepted 7 October 2013

Academic Editor: Yong Jiang

Copyright © 2013 Letizia Mezzasoma et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Postoperative-fluid retention is a severe complication frequently reported in patients undergoing major surgical procedures. The complex network of molecules involved in such a severe surgery-induced condition remains poorly understood. Inflammation has been proposed among the various causes of fluid retention. Since TNF-α is one of the main proinflammatory cytokine initially released after major surgery, it is reasonable to assume its involvement in fluid overload. Here, we showed that TNF-α selectively regulates key molecules involved in fluids balance, such as natriuretic peptides (NPs) and aquaporins, in human bronchial epithelial cells BEAS-2B. In particular, we found that TNF-α induced a decrease of arial natriuretic peptide, natriuretic peptide receptor-1, aquaporin-1 and aquaporin-5 and an increase of brain natriuretic peptide with a different involvement of nuclear factor-κB and mitogen-activated protein kinases signaling pathway activation. Moreover, the observed changes in NPs expression, demonstrate inflammation as an additional cause of brain natriuretic peptide elevation, adding an important piece of information in the novel area of study regarding NPs and inflammation. Finally, we suggest that inflammation is one of the mechanisms of Aquaporin-1 and aquaporin-5 expression regulation. Therefore, in this exploratory study, we speculate that TNF-α might be involved in postoperative-fluid retention related to major surgery.