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Am J Physiol Cell Physiol 287: C939-C948, 2004. First published June 2, 2004; doi:10.1152/ajpcell.00413.2003
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MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

Modulation of chloride secretory responses and barrier function of intestinal epithelial cells by the Salmonella effector protein SigD

Lone S. Bertelsen,1 Günther Paesold,1 Sandra L. Marcus,2 Brett B. Finlay,2 Lars Eckmann,1 and Kim E. Barrett1

1Department of Medicine, Division of Gastroenterology, University of California-San Diego School of Medicine, San Diego, California 92103-8414; and 2Biotechnology Laboratory, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3

Submitted 26 September 2003 ; accepted in final form 31 May 2004

The Salmonella effector protein SigD is an inositol phosphate phosphatase that inhibits phosphatidylinositol 3-kinase-dependent signaling. Because epidermal growth factor (EGF) inhibits chloride secretion via phosphatidylinositol 3-kinase, we explored whether Salmonella infection might modify the inhibitory effect of EGF. As expected, EGF inhibited chloride secretion induced by carbachol in T84 epithelial cells. Infection with wild-type (WT) but not sigD– mutant S. typhimurium SL1344 decreased CCh-stimulated chloride secretion. Moreover, WT but not sigD– Salmonella reduced the inhibitory effect of EGF on carbachol-stimulated chloride secretion. Complementation of sigD restored the ability of mutant Salmonella to reverse the inhibitory effect of EGF. EGF-induced EGF receptor phosphorylation was similar in cells infected with either WT or mutant Salmonella, and neither WT nor sigD– Salmonella altered recruitment of the p85 subunit of phosphatidylinositol 3-kinase to EGF receptor, implying that SigD acts downstream of these signaling events. Furthermore, transepithelial resistance fell more rapidly in cells infected with WT vs. sigD– Salmonella, indicating an early role for SigD in reducing barrier function, perhaps via activation of protein kinase C. We conclude that the Salmonella bacterial effector protein SigD may play critical roles in the pathogenesis of disease caused by this microorganism.

chloride secretion; Salmonella typhimurium; epidermal growth factor


Address for reprint requests and other correspondence: K. E. Barrett, Division of Gastroenterology, UCSD Medical Center, 8414, 200 W. Arbor Dr. (for courier delivery, use CTF-A109, 210 Dickinson St.), San Diego, CA 92103-8414 (E-mail: kbarrett{at}ucsd.edu)




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