Inhibition and redistribution of NHE3, the apical Na+/H+ exchanger, by Clostridium difficile toxin B.
Ontology highlight
ABSTRACT: NHE3, the apical isoform of the Na(+)/H(+) exchanger, is central to the absorption of salt and water across the intestinal epithelium. We report that treatment of epithelial cells with toxin B of Clostridium difficile, a diarrheal pathogen, causes a pronounced inhibition of NHE3 activity, with little effect on the basolateral NHE1 isoform. Depression of NHE3 activity is accompanied by the translocation of apical exchangers to a subapical endomembrane compartment. Treatment of cells with toxin B increased the fraction of exchangers that were solubilized by nonionic detergents and induced dephosphorylation and extensive redistribution of ezrin. The Rho-kinase inhibitor, Y-27632, also altered the distribution and activity of NHE3. We suggest that inactivation of Rho-family GTPases by clostrid
SUBMITTER: Hayashi H
PROVIDER: S-EPMC2234495 | biostudies-literature | 2004 May
REPOSITORIES: biostudies-literature
ACCESS DATA