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Infection and Immunity, February 1999, p. 745-753, Vol. 67, No. 2
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Increased Type 1 Fimbrial Expression among Commensal Escherichia coli Isolates in the Murine Cecum following Catabolic Stress

Barbara A. Hendrickson,1,* Jun Guo,1 Robert Laughlin,2 Yimei Chen,3 and John C. Alverdy2

Section of Infectious Diseases, Department of Pediatrics, University of Chicago Children's Hospital,1 and Department of Surgery2 and Department of Molecular Genetics and Cell Biology,3 University of Chicago, Chicago, Illinois

Received 28 August 1998/Returned for modification 20 October 1998/Accepted 24 November 1998

Although indigenous bacteria intimately colonize the intestinal mucosa, under normal conditions the intestinal epithelial cell is free of adherent bacteria. Nonetheless, commensal bacteria such as Escherichia coli adhere to and translocate across the intestinal epithelium in association with a number of pathologic states including hemorrhagic shock, immunosuppression, traumatic tissue injury, and lack of enteral feedings. The adhesins involved in the adherence of indigenous E. coli to the intestinal epithelium in vivo following catabolic stress are unknown. We have developed a mouse model to study the bacterial adhesins which mediate the increased intestinal adherence of E. coli after partial hepatectomy and short-term starvation. Our studies demonstrated that hepatectomy and starvation in the mouse were associated with a 7,500-fold increase in the numbers of E. coli bacteria adhering to the cecum. In addition, erythrocyte agglutination studies, as well as immunostaining of fimbrial preparations and electron micrographs of the bacteria, revealed that surface type 1 fimbriae were more abundant in the commensal E. coli harvested from the ceca of the stressed mice. These E. coli isolates adhered to a mouse colon cell line and injected cecal loops in a mannose-inhibitable manner, which suggests a role for type 1 fimbriae in the adherence of the E. coli isolates to the cecum in vivo following host catabolic stress.

* Corresponding author. Mailing address: Section of Pediatric Infectious Diseases, University of Chicago Children's Hospital, 5841 S. Maryland Ave.---MC6054, Chicago, IL 60637. Phone: (773) 702-6176. Fax: (772) 702-1196. E-mail: bhendric{at}peds.bsd.uchicago.edu.

Infection and Immunity, February 1999, p. 745-753, Vol. 67, No. 2
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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