Tumor Necrosis Factor-α Selectively Regulates Natriuretic Peptides and Aquaporins in Human Bronchial Epithelial Cells BEAS-2B.

Inflammation has been proposed among the causes of postoperative-fluid retention, a severe complication frequently reported in patients undergoing major surgical procedures. Here we showed that Tumor Necrosis Factor-α (TNF‐α), one of the main pro-inflammatory cytokines early released after major surgery, selectively regulates key molecules involved in fluids balance, such as Natriuretic Peptides (NPs) and Aquaporins (AQPs), in human bronchial epithelial cells BEAS-2B. In particular, TNF-α treatment induced a decrease of Atrial Natriuretic Peptide (ANP) mRNA level, an increase of Brain Natriuretic Peptide (BNP) mRNA and protein levels, and a down-regulation of AQP1 and AQP5 mRNA expression. The selective modulation of NPs and AQPs gene expression after TNF-α treatment appeared to be related to a different involvement of Nuclear Factor-kB (NF-kB) signaling pathway activation. Moreover, the observed changes in NPs expression, occurring here independently from hemodynamic influences, suggested that inflammation should be considered an additional cause of BNP elevation, adding an important piece of information in the novel area of study regarding NPs and inflammation. Finally, we suggested inflammation among the mechanisms of AQP1 and AQP5 expression regulation. Taken together our results support the idea of inflammation involvement in postoperative fluid retention related to major surgery.