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Am J Physiol Gastrointest Liver Physiol 291: G959-G968, 2006. First published June 15, 2006; doi:10.1152/ajpgi.00274.2005
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HORMONES AND SIGNALING

Rapid activation of Na+/H+ exchange by EPEC is PKC mediated

Kim Hodges, Ravinder Gill, K. Ramaswamy, Pradeep K. Dudeja,* and Gail Hecht*

Section of Digestive Disease and Nutrition, Department of Medicine, University of Illinois at Chicago and Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois

Submitted 15 June 2005 ; accepted in final form 7 June 2006

Enteropathogenic Escherichia coli (EPEC) increases sodium/hydrogen exchanger 2 (NHE2)-mediated sodium uptake by intestinal epithelial cells in a type III secretion-dependent manner. However, the mechanism(s) underlying these changes are not known. This study examines the role of a number of known secreted effector molecules and bacterial adhesins as well as the signaling pathways involved in this process. Deletion of the bacterial adhesins Tir and intimin had no effect on the increase in sodium/hydrogen exchanger (NHE) activity promoted by EPEC infection; however, there was a significant decrease upon deletion of the bundle-forming pili. Bacterial supernatant also failed to alter NHE activity, suggesting that direct interaction with bacteria is necessary. Analysis of the signal transduction cascades responsible for the increased NHE2 activity during EPEC infection showed that PLC increased Ca2+, as well as PKC{alpha} and PKC{epsilon} were involved in increasing NHE activity. The activation of PKC{epsilon} by EPEC has not been previously described nor has its role in regulating NHE2 activity. Because EPEC markedly increases NHE2 activity, this pathogen provides an exceptional opportunity to improve our understanding of this less-characterized NHE isoform.

sodium/hydrogen exchanger; enteropathogenic Escherichia coli; protein kinase C; epsilon; alpha


Address for reprint requests and other correspondence: G. Hecht, Digestive Diseases and Nutrition, Univ. of Illinois, Clinical Science Bldg. (MC 716), #704, 840 S. Wood St., Chicago, IL 60612 (e-mail: gahecht{at}uic.edu)






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