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1 Medicine, University of California, San Diego, School of Medicine, San Diego, CA, USA; Biotechnology Laboratory, University of British Columbia, Vancouver, BC, Canada
* To whom correspondence should be addressed. E-mail: kbarrett{at}ucsd.edu.
The Salmonella effector protein, SigD, is an inositol phosphate phosphatase that inhibits phosphatidylinositol 3-kinase (PI 3-K) dependent signaling. Because epidermal growth factor (EGF) inhibits chloride secretion via PI 3-K, we explored whether Salmonella infection might modify the inhibitory effect of EGF. As expected, EGF inhibited chloride secretion induced by carbachol (CCh) 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 CCh-stimulated chloride secretion. Complementation of sigD restored the ability of mutant Salmonella to reverse the inhibitory effect of EGF. EGF-induced EGF receptor (EGFr) 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 PI 3-K to EGFr, implying SigD acts downstream of these signaling events. Further, transepithelial resistance fell more rapidly in cells infected with WT versus 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.
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