This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Johnson, A. M.
Right arrow Articles by Hardwidge, P. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Johnson, A. M.
Right arrow Articles by Hardwidge, P. R.

 Previous Article  |  Next Article 

Infection and Immunity, January 2009, p. 341-347, Vol. 77, No. 1
0019-9567/09/$08.00+0     doi:10.1128/IAI.01097-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Enterotoxigenic Escherichia coli Modulates Host Intestinal Cell Membrane Asymmetry and Metabolic Activity{triangledown}

Amber M. Johnson, Radhey S. Kaushik, Nicholas J. Rotella, and Philip R. Hardwidge*

Center for Infectious Disease Research and Vaccinology, South Dakota State University, Brookings, South Dakota

Received 2 September 2008/ Returned for modification 6 October 2008/ Accepted 13 October 2008

Enterotoxigenic Escherichia coli (ETEC) is a common cause of travelers' and postweaning diarrhea in humans and swine, respectively. The extent to which ETEC damages host cells is unclear. Experiments are presented that probe the ability of porcine ETEC isolates to induce apoptosis and cell death in porcine intestinal epithelial cells. Quantification of host phosphatidylserine exposure following ETEC infection suggested that ETEC induced changes in plasma membrane asymmetry, independent of the expression of the heat-labile enterotoxin. Significant host cell death was not observed. ETEC infection also caused a drastic inhibition of host esterase activity, as measured by calcein fluorescence. While ETEC infection resulted in activation of host caspase 3, terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling of DNA double-strand breakage, indicative of late stages of apoptosis, was not observed. Camptothecin-induced apoptosis markedly increased subsequent ETEC adherence. Transfer of cell-free supernatants from apoptotic cells to bacterial inocula prior to infection of naïve cells increased the transcriptional activity of the regulatory region upstream of the K88ac operon and promoted subsequent adherence to host cells.

* Corresponding author. Mailing address: South Dakota State University, Box 2175, 1119 North Campus Drive, Brookings, SD 57007. Phone: (605) 688-5259. Fax: (605) 688-6003. E-mail: hardwidg{at}gmail.com

{triangledown} Published ahead of print on 20 October 2008.

Editor: B. A. McCormick

Infection and Immunity, January 2009, p. 341-347, Vol. 77, No. 1
0019-9567/09/$08.00+0     doi:10.1128/IAI.01097-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Ghosal, A., Bhowmick, R., Banerjee, R., Ganguly, S., Yamasaki, S., Ramamurthy, T., Hamabata, T., Chatterjee, N. S. (2009). Characterization and Studies of the Cellular Interaction of Native Colonization Factor CS6 Purified from a Clinical Isolate of Enterotoxigenic Escherichia coli. Infect. Immun. 77: 2125-2135 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»