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Infection and Immunity, May 1999, p. 2209-2217, Vol. 67, No. 5
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Shiga Toxin 1 from Escherichia coli Blocks Activation and Proliferation of Bovine Lymphocyte Subpopulations In Vitro

C. Menge,1,* L. H. Wieler,1,2 T. Schlapp,1,3 and G. Baljer1

Institut für Hygiene und Infektionskrankheiten der Tiere der Justus-Liebig-Universität, Giessen, D-35392 Giessen,1 Institut für Mikrobiologie und Tierseuchen der Freien Universität Berlin, D-10115 Berlin,2 and Institut für Infektionskrankheiten, Bayer AG, Gebäude 6210/Monheim, D-51368 Leverkusen,3 Germany

Received 8 September 1998/Returned for modification 15 October 1998/Accepted 24 February 1999

Shiga toxin-producing Escherichia coli (STEC) is widespread in the cattle population, but the clinical significance of Shiga toxins (Stx's) for the bovine species remains obscure. Since Stx's exert immunomodulating effects in other species, we examined the effect of purified Stx1 on a bovine B lymphoma cell line (BL-3) and peripheral blood mononuclear cells (PBMC) isolated from adult bovine blood by viability assays and flow cytometry analysis. Stx1 markedly induced apoptosis in stimulated BL-3 cells. The susceptibility of this B-cell-derived cell line was induced only by either lipopolysaccharide (LPS) or pokeweed mitogen, while cultures stimulated with T-cell mitogens were unaffected by the toxin. In contrast, Stx1 did not induce cellular death---neither apoptosis nor necrosis---in primary cultures of PBMC but hindered the mitogen-induced increase in metabolic activity. The influence of Stx1 on single PBMC subpopulations varied with the type of mitogenic stimulus applied. Stimulation with phytohemagglutinin P particularly induced the proliferation of bovine CD8-expressing (BoCD8+) cells, and this proliferative response was blocked by Stx1. On the other hand, Stx1 reduced the portion of viable B cells in the presence of LPS. Modulation of activation marker expression (BoCD25 and BoCD71) by Stx1 indicated that the toxin hindered the proliferation of cells by blocking their activation. In conclusion, we assume that Stx1 contributes to the pathogenesis of STEC-associated diarrhea in calves by suppressing the mucosa-associated immune response. The usefulness of cattle as a model in which to study Stx-induced immunomodulation is discussed.

* Corresponding author. Mailing address: Institut für Hygiene und Infektionskrankheiten der Tiere, Frankfurter Str. 89, D-35392 Giessen, Germany. Phone: 49-641-99-38314. Fax: 49-641-99-38309. E-mail: christian.menge{at}vetmed.uni-giessen.de.

Infection and Immunity, May 1999, p. 2209-2217, Vol. 67, No. 5
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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