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In vivo RNA-sequencing of Vibrio cholerae during intestinal colonization of infant rabbits

ABSTRACT: To understand how cholera toxin (CT) produced by Vibrio cholerae modulates gene expression of this organism within the intestine, RNA-seq analysis was performed on two samples each of WT and the ∆ctx mutant bacteria harvested from either the infant rabbit ileum or the cecum one-day post-intragastric infection. We found that 243 genes that were significantly up-regulated in the WT compared to the ∆ctx mutant and these included 101 genes in ileum samples, 118 in the cecum samples, and 24 in both samples. We found that genes known to be induced under low-iron growth conditions were up-regulated in WT relative to the ∆ctx mutant in both the ileum and in the cecum, with a marked up-regulation in the ileum relative to the cecum. We also found that genes involved in TCA cycle metabolism, L-Lactate utilization, and LCFA utilization were significantly up-regulated in the WT in the ileum relative to the ∆ctx mutant during infection. We conclude that CT-induced disease creates an iron-depleted metabolic niche in the gut that modulates the transcriptional profile of this pathogen during infection.

ORGANISM(S): Vibrio cholerae

PROVIDER: GSE132653 | GEO | 2019/07/31

REPOSITORIES: GEO

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Project description:Adherence of pathogenic Escherichia coli strains to intestinal epithelia is essential for infection. For enterohemorrhagic E. coli (EHEC) serotype O157:H7, we have previously demonstrated that multiple factors govern this pathogen’s adherence to HeLa cells (39). One of these factors is CadA, a lysine decarboxylase, and this protein has been proposed to negatively regulate virulence in several enteric pathogens. In the case of EHEC strains, CadA modulates expression of the intimin, an outer membrane adhesin involved in pathogenesis. Here, we experimentally inactivated cadA in O157:H7 strain 86-24 to investigate the role of this gene in EHEC adhesion to tissue culture monolayers, global gene expression patterns, and colonization of the infant rabbit intestine. As expected, the cadA mutant did not possess lysine decarboxylation activity and was hyper-adherent to tissue-culture cells. Adherence of the cadA mutant was nearly 2-fold greater than that of the wt and complementation of the cadA defect reduced adherence back to wt levels. Furthermore, the cadA mutant affected the expression of intimin protein. Disruption of the eae gene (encoding the intimin protein) in the cadA mutant significantly reduced its adherence to tissue-culture cells. However, adherence of the cadA eae double mutant was greater than that of an 86-24 eae mutant, suggesting that the enhanced adherence of the cadA mutant is not entirely attributable to enhanced expression of intimin in this background. Gene array analysis revealed that the cadA mutation significantly altered EHEC gene expression patterns; expression of 1332 genes was down-regulated and 132 genes up-regulated in the mutant compared to the wild type strain. Interestingly, the gene expression variation shows an EHEC-biased gene alteration including intergenic regions. Two putative adhesins: flagella and F9 fimbriae were up-regulated in the cadA mutant, suggestive of their association with adherence in absence of the Cad regulatory mechanism. Remarkably, in the infant rabbit model, the cadA mutant out-competed the wild type strain in the ileum but not in the cecum or mid-colon, raising the possibility that CadA negatively regulates EHEC pathogenicity in a tissue-specific fashion.

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In vivo RNA-sequencing of Vibrio cholerae during intestinal colonization of infant rabbits

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