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Downregulation of ENaC activity and expression by TNF- in alveolar epithelial cells

Centre de recherche, Centre hospitalier de l'Université de Montréal-Hôtel-Dieu, and Département de médecine, Université de Montréal, Montreal, Quebec, Canada H2W 1T7

Submitted 25 September 2002 ; accepted in final form 20 September 2003

Sodium absorption by an amiloride-sensitive channel is the main driving force of lung liquid clearance at birth and lung edema clearance in adulthood. In this study, we tested whether tumor necrosis factor- (TNF-), a proinflammatory cytokine involved in several lung pathologies, could modulate sodium absorption in cultured alveolar epithelial cells. We found that TNF- decreased the expression of the -, -, and -subunits of epithelial sodium channel (ENaC) mRNA to 36, 43, and 16% of the controls after 24-h treatment and reduced to 50% the amount of -ENaC protein in these cells. There was no impact, however, on ₁ and ₁ Na⁺-K⁺-ATPase mRNA expression. Amiloride-sensitive current and ouabain-sensitive Rb⁺ uptake were reduced, respectively, to 28 and 39% of the controls. A strong correlation was found at different TNF- concentrations between the decrease of amiloride-sensitive current and -ENaC mRNA expression. All these data show that TNF-, a proinflammatory cytokine present during lung infection, has a profound influence on the capacity of alveolar epithelial cells to transport sodium.

sodium ion channel; transepithelial current; cytokine; inflammation

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