Sodium absorption by the amiloride-sensitive epithelial sodium channel (ENaC) is the main driving force involved in lung edema clearance. Recently, the regulation of this sodium transport mechanism in injured lung is evaluated [1]. There is accumulating evidence that the expression level of ENaC is modulated in injured lungs. In a chronic Pseudomonas aeruginosa lung infection model, we observed a distinctive expression profile for the three subunits (α, β and γENaC) [2]. All the subunits showed an increased expression at 24h post infection followed by a decrease on day 3. In a model of ischemia-reperfusion lung injury (single lung transplantation), we also observed a decreased expression of ENaC mRNA in the transplanted lungs [3]. Furthermore, we found that alveolar liquid clearance was significantly lower in transplanted lungs and that alveolar liquid clearance could not be stimulated β-adrenergic agonist. Although the mechanism involved in this downregulation of ENaC expression is not known at the moment, we propose that inflammatory mediators could potentially be involved. In fact, TNFα a pro-inflammatory cytokine involved in these lung injury models decrease the expression of the α, β and γENaC mRNA subunits and had a major impact on the transepithelial current generated by the alveolar epithelial cells [4]. Our recent data also shows that other inflammatory molecules like LPS from P. aeruginosa modulate ENaC expression and activity in alveolar epithelial cells. We were able to show that this effect of LPS involves the release of ATP from alveolar epithelial cells and is most likely associated with a stimulation of the purinergic receptor (P2Y2) [5]. Can this effect of inflammatory molecules on ENaC expression and activity be inhibited by anti-inflammatory treatment? Because the synthetic steroid dexamethasone has been shown to upregulate ENaC mRNA expression [6], and is well-known to downregulate pro-inflammatory genes, we tested if it could alleviate the effect of TNF on ENaC expression and activity. In co-treatment with TNF, we found that dexamethasone reversed the inhibitory effect of TNF and upregulated α, β and γENaC mRNA expression [7]. In addition to its effect on αENaC gene expression, dexamethasone was able to maintain amiloride-sensitive current as well as the liquid clearance abilities of TNF-treated cells within the normal range. All these results suggest that dexamethasone alleviates the downregulation of ENaC expression and activity in TNF-treated alveolar epithelial cells. Overall, these data suggest that ENaC expression in injured lung can be modulate by inflammatory molecules. The impact of theses changes in expression on the evolution of lung injury remains to be determined.