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Clinical and Diagnostic Laboratory Immunology, May 2004, p. 548-551, Vol. 11, No. 3
1071-412X/04/$08.00+0     DOI: 10.1128/CDLI.11.3.548-551.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Interleukin-8 Response in an Intestinal HCT-8 Cell Line Infected with Enteroaggregative and Enterotoxigenic Escherichia coli

David B. Huang,1,2 Herbert L. DuPont,1,2,3,4 Zhi-Dong Jiang,2 Lily Carlin,3 and Pablo C. Okhuysen2,3*

Department of Medicine, Baylor College of Medicine,1 University of Texas at Houston School of Public Health,2 University of Texas at Houston Medical School,3 St. Luke's Episcopal Hospital, Houston, Texas4

Received 8 December 2003/ Returned for modification 12 January 2004/ Accepted 23 January 2004

This study examined the interleukin-8 (IL-8) response of the intestinal adenocarcinoma HCT-8 cell line to infection with enteroaggregative and enterotoxigenic Escherichia coli pathotypes isolated from patients with travelers' diarrhea. Individual diarrheagenic E. coli strains (enteroaggregative E. coli [EAEC]; n = 30), heat-stable enterotoxin (ST)-producing enterotoxigenic E. coli (ETEC ST; n = 11), heat-labile enterotoxin (LT)-producing enterotoxigenic E. coli (ETEC LT; n = 10), and ST- and LT-producing enterotoxigenic E. coli (ETEC ST:LT; n = 8) were coincubated with HCT-8 cells for 3 h. Tissue culture supernatants were assayed for IL-8 content by enzyme-linked immunosorbent assay. Fifty percent of EAEC (72% of those EAEC carrying the virulence factors aggR, aggA, and aspU and 40% of those EAEC not carrying virulence factors) and 64% of ETEC ST elicited IL-8 production. In contrast, 10% of ETEC LT elicited the production of IL-8 above baseline. These results suggest that (i) the HCT-8 cell line infection model can be used as a tool to differentiate proinflammatory E. coli from noninflammatory isolates; (ii) EAEC has a heterogeneous ability to induce the production of IL-8, and this may be associated with the presence of virulence factors; and (iii) ETEC ST can elicit an inflammatory response and helps explain our earlier findings of increased fecal IL-8 in patients with ETEC diarrhea.


* Corresponding author. Mailing address: University of Texas Health Science Center, Houston Medical School, 6431 Fannin, JFB 1.728, Houston, TX 77030. Phone: (713) 500-6736. Fax: (713) 500-5495. E-mail: Pablo.c.okhuysen{at}uth.tmc.edu.


Clinical and Diagnostic Laboratory Immunology, May 2004, p. 548-551, Vol. 11, No. 3
1071-412X/04/$08.00+0     DOI: 10.1128/CDLI.11.3.548-551.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.




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