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University of Balamand > Academics > Research > Seminars > Omar Itani

Analysis of the Higher Voltage in the Cystic Fibrosis Airway

Thursday, December 4, 2008 from 12:30 PM till 2:00 PM at the Jacobo Auditorium

SUBMITTED BY: Dr. Omar Itani
University of Balamand
Faculty of Sciences

ABSTRACT: Lung disease in cystic fibrosis (CF) is caused by loss of CFTR, a Cl- channel expressed in airway epithelia. A hallmark of CF is an increased transepithelial voltage (Vt) across airway epithelia. The basis for the elevated Vt is not understood, but is often attributed to increased epithelial sodium channel (ENaC) activity. To determine the mechanism responsible for the higher Vt, we tested three hypotheses. First, we tested the hypothesis that CF submucosal glands generate a higher voltage that increases Vt. Consistent with this idea, the distribution of submucosal glands in mice paralleled the Vt differences. However, submucosal glands had a low voltage in CF and non-CF mice. Second, we asked if CF airways have increased Na+ current. In well-differentiated human airway epithelial cultures, we found similar ENaC act​ivity in CF and non-CF epithelia. Third, we tested the hypothesis that loss of CFTR Cl- channels increases transepithelial resistance (Rt) thereby increasing Vt. Data from CF and non-CF epithelia were consistent with this hypothesis. Moreover, pharmacologically blocking CFTR increased Vt in cultured non-CF epithelia and mouse epithelia in vivo, but had no effect in CF epithelia or mice. These data suggest that the higher Vt in CF compared to non-CF epithelia results from a higher Rt in CF airway epithelia. These results have important implications for understanding CF pathogenesis and approaches to therapy.
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