We previously developed a swine animal model in which natural host resistance to Campylobacter jejuni is altered by experimental infection with low numbers of the nematode Trichuris suis. Pigs naturally colonized with C. jejuni experience colitis because of the invasion of the bacterium approximately 21 days after exposure to T. suis. To better understand the mechanism of T. suis–dependent C. jejuni colitis, we evaluated the effects of T. suis excretory–secretory products (ESPs) on intestinal epithelial cells (IECs) and the influence of ESP on C. jejuni invasion in IECs under in vitro conditions. Viability assays revealed a dose-dependent cytotoxic response in ESP-treated IECs, particularly IPEC-1 and INT407 cells. Transepithelial electrical resistance dropped significantly in IPEC-1 cells treated on apical and basolateral surfaces, but not in those treated only on apical surfaces. Using the gentamicin-killing assay, reduced numbers of intracellular C. jejuni were recovered from IECs treated with ESP at 1 mg protein/ml concentration. This observation can be at least partially explained by a novel antibacterial activity in ESP. Contrary to our hypothesis, ESP at subtoxic concentrations did not enhance invasion. In addition to mechanical damage from worms, these results suggest that soluble products released by T. suis contribute to IEC damage at the site of worm attachment.
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