Abstract
BackgroundPreviously we found that E. coli O157:H7 inoculated into ligated pig intestine formed attaching and effacing (AE) lesions in some pigs but not in others. The present study evaluated changes in the microbial community and in virulence gene expression in E. coli O157:H7 in ligated pig intestine in which the bacteria formed AE lesions or failed to form AE lesions.Methodology/Principal FindingsThe intestinal microbiota was assessed by RNA-based denaturing gradient gel electrophoresis (DGGE) analysis. The DGGE banding patterns showed distinct differences involving two bands which had increased intensity specifically in AE-negative pigs (AE- bands) and several bands which were more abundant in AE-positive pigs. Sequence analysis revealed that the two AE- bands belonged to Veillonella caviae, a species with probiotic properties, and Bacteroides sp. Concurrent with the differences in microbiota, gene expression analysis by quantitative PCR showed that, compared with AE negative pigs, E. coli O157:H7 in AE positive pigs had upregulated genes for putative adhesins, non-LEE encoded nleA and quorum sensing qseF, acid resistance gene ureD, and genes from the locus of enterocyte effacement (LEE).Conclusions/SignificanceThe present study demonstrated that AE-positive pigs had reduced activities or populations of Veillonella caviae and Bacterioides sp. compared with AE-negative pigs. Further studies are required to understand how the microbiota was changed and the role of these organisms in the control of E. coli O157:H7.
Highlights
Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is an enteric pathogen that causes foodborne disease ranging from uncomplicated diarrhea to hemorrhagic colitis (HC) and lifethreatening hemolytic uremic syndrome (HUS) in humans [1]
Two major virulence factors are involved in causing disease: products of a pathogenicity island named the locus of enterocyte effacement (LEE), that are needed for intestinal colonization, and Shiga toxin (Stx) which causes damage to tissues [2]
We have shown that E. coli O157:H7 grown in MacConkey broth and exposed to pH 2.5 had little or no adherence to intestinal epithelial cells in vitro, but caused significant adherence and AE lesions when inoculated into pig intestinal loops [10, 11], suggesting that the intestinal environment, including the microbiota, favors the expression and secretion of virulence factors for infection and AE lesion [5, 10, 12]
Summary
Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is an enteric pathogen that causes foodborne disease ranging from uncomplicated diarrhea to hemorrhagic colitis (HC) and lifethreatening hemolytic uremic syndrome (HUS) in humans [1]. We have shown that E. coli O157:H7 grown in MacConkey broth and exposed to pH 2.5 had little or no adherence to intestinal epithelial cells in vitro, but caused significant adherence and AE lesions when inoculated into pig intestinal loops [10, 11], suggesting that the intestinal environment, including the microbiota, favors the expression and secretion of virulence factors for infection and AE lesion [5, 10, 12]. The present study evaluated changes in the microbial community and in virulence gene expression in E. coli O157:H7 in ligated pig intestine in which the bacteria formed AE lesions or failed to form AE lesions
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