1887

Abstract

Ruminants are a major reservoir of enterohaemorrhagic (EHEC), which cause acute gastroenteritis in humans with potentially life-threatening sequelae. The mechanisms underlying EHEC persistence in ruminant hosts are poorly understood. EHEC produce several cytotoxins that inhibit the proliferation of bovine lymphocytes and influence EHEC persistence in calves, suggesting that bacterial suppression of mucosal inflammation may be important . In order to address this hypothesis, intraepithelial lymphocytes (IEL) obtained from ligated intestinal loops of five 9–14 day old calves were characterized 12 h after inoculation with strains. Loops were inoculated with an EHEC O103 : H2 strain, an isogenic Δ mutant incapable of producing Shiga toxin 1 (Stx1) and a porcine non-pathogenic strain. The IEL mainly comprised activated CD2 CD3 CD6 CD8α T cells and resembled IEL obtained from the intestinal mucosa of orally challenged calves. Forty per cent of all IEL were potentially sensitive to Stx1 in that they expressed the receptor for Stx1. Nevertheless, analysis of IEL from inoculated loops failed to detect a significant effect of the different strains on proliferative capacity, natural killer cell activity or the cytokine mRNA profile. However, the EHEC wild-type strain reduced the percentage of CD8α T cells in the ileal mucosa compared with loops inoculated with the Δ mutant. This shift in IEL composition was not associated with inhibition of IEL proliferation , since the majority of the IEL from all loops were in the G/G phase of the cell cycle. These studies indicate that the ligated ileal loop model will be a useful tool to dissect the mechanisms underlying suppression of mucosal inflammation by EHEC in the reservoir host.

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2004-06-01
2024-04-23
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