Abstract
We established an automated screening method to characterize adhesion of Escherichia coli to intestinal porcine epithelial cells (IPEC-J2) and their probiotic activity against infection by enteropathogenic E. coli (EPEC). 104 intestinal E. coli isolates from domestic pigs were tested by PCR for the occurrence of virulence-associated genes, genes coding for resistances to antimicrobial agents and metals, and for phylogenetic origin by PCR. Adhesion rates and probiotic activity were examined for correlation with the presence of these genes. Finally, data were compared with those from 93 E. coli isolates from wild boars.Isolates from domestic pigs carried a broad variety of all tested genes and showed great diversity in gene patterns. Adhesions varied with a maximum of 18.3 or 24.2 mean bacteria adherence per epithelial cell after 2 or 6 hours respectively. Most isolates from domestic pigs and wild boars showed low adherence, with no correlation between adhesion/probiotic activity and E. coli genes or gene clusters. The gene sfa/foc, encoding for a subunit of F1C fimbriae did show a positive correlative association with adherence and probiotic activity; however E. coli isolates from wild boars with the sfa/foc gene showed less adhesion and probiotic activity than E. coli with the sfa/foc gene isolated from domestic pigs after 6 hour incubation.In conclusion, screening porcine E. coli for virulence associated genes genes, adhesion to intestinal epithelial cells, and probiotic activity revealed a single important adhesion factor, several probiotic candidates, and showed important differences between E. coli of domestic pigs and wild boars.
Highlights
Intestinal bacterial communities are very complex and individual
We showed that E. coli Nissle 1917 (EcN) and another F1C fimbriae-positive E. coli isolate from a wild boar inhibited Salmonella adhesion and invasion
We investigated a large cohort of intestinal E. coli isolates from domestic pigs and wild boars for the first time to address the probiotic phenomenon
Summary
Bacteria exist in specific microhabitats and metabolic niches, which are defined by the host (e.g., epithelial cells, mucus, peristaltic activity, pH), nutrition and the microbiota itself. An ingested pathogen must compete with the normal microbiota and can preferentially infect the host if an intestinal niche is unoccupied by another bacteria, or can outcompete an established bacteria in its niche. It is reasonable that bacteria of the normal microbiota may inhibit infections by intestinal pathogens if they can out-compete the pathogen for a particular niche. E. coli has been shown to inhibit intestinal infection by certain pathogens [1,2,3]. Such an inhibiting effect is known as a ‘‘probiotic’’ effect
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