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The role of the Cj0440c gene in erythromycin-resistant (Eryr) Campylobacter jejuni

ABSTRACT: Cj0440c, a putative transcriptional regulator, was over-expressed in the high-level erythromycin-resistant (Eryr) Campylobacter jejuni strains. To determine the role of Cj0440c on the development and fitness of erythromycin resistance in C. jejuni, we knocked out Cj0440c in Eryr strain (R) to obtain the Cj0440c mutants (RM). Then we compared the transcriptome of the Cj0440c mutant with that of the parent strain using DNA microarray. These comparisons identified 9 genes that showed a ≥2-fold change in expression in RM. The differentially expressed genes in RM are related to flagellar biosynthesis and unknown functions. What's more, katA, encoding catalase, down-regulated in RM. Cj0440c may progress flagellar genes expression, help to escape drug pressure and disseminate and colonize smoothly, and Cj0440c in Eryr Campylobacter may protect bacteria from harmful oxygen stress from the host immune system, other microorganism in host intestinal and its own products. These findings indicate that Cj0440c is essential for the fitness (growth) of resistant C. jejuni by controlling the expression of several genes involved in flagellar assembly and catalase, enhancing cell motility for colonization and invasion under the pressure of drug. This study widened our understanding on the molecular mechanism of resistance and provides scientific reference for drug research and application.

ORGANISM(S): Campylobacter jejuni subsp. jejuni NCTC 11168 = ATCC 700819

PROVIDER: GSE49255 | GEO | 2013/08/13

SECONDARY ACCESSION(S): PRJNA214941

REPOSITORIES: GEO

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Project description:Campylobacter jejuni is a prevalent cause of bacterial gastroenteritis in humans worldwide. The mechanism by which C. jejuni survives stomach acidity remains unknown. Herein, we have demonstrated that C. jejuni with a fur deletion was more sensitive to acid than the wild-type strain. Profiling the acid stimulon of the C. jejuni ∆fur mutant allowed us to uncover Fur-regulated genes under acidic conditions. The up-regulation of heat shock genes and the down-regulation of genes involved in flagellar and cell envelope biogenesis in the fur mutant highlight the importance of Fur in Campylobacter acid survival. Interestingly, prior acid exposure of C. jejuni cross-protected the bacterium against oxidative stress. Western-blot analysis and real-time qRT-PCR revealed an increased expression of the catalase KatA in acid-stressed C. jejuni relative to unstressed bacteria. The enhanced survival of C. jejuni to oxidative stress was shown to be Fur-dependent through the regulation of katA expression. Electrophoretic mobility shift assay (EMSA) demonstrated that the binding affinity between Fur and katA is reduced under low pH allowing for higher expression of katA and the defense against oxidative stress. Strikingly, the ∆fur mutant exhibited a reduced virulence capacity in both human epithelial cells and G. mellonella infection model as compared to C. jejuni wild-type. Altogether, this is the first study showing that in addition to its role in iron metabolism, Fur is an important regulator of C. jejuni acid response and cross-protection against other stresses. Moreover, our results clearly demonstrate that Fur plays a substantial role in C. jejuni host pathogenesis. Campylobacter jejuni is a prevalent cause of bacterial gastroenteritis in humans worldwide. The mechanism by which C. jejuni survives stomach acidity remains unknown. Herein, we have demonstrated that C. jejuni with a fur deletion was more sensitive to acid than the wild-type strain. Profiling the acid stimulon of the C. jejuni ∆fur mutant allowed us to uncover Fur-regulated genes under acidic conditions. The up-regulation of heat shock genes and the down-regulation of genes involved in flagellar and cell envelope biogenesis in the fur mutant highlight the importance of Fur in Campylobacter acid survival. Interestingly, prior acid exposure of C. jejuni cross-protected the bacterium against oxidative stress. Western-blot analysis and real-time qRT-PCR revealed an increased expression of the catalase KatA in acid-stressed C. jejuni relative to unstressed bacteria. The enhanced survival of C. jejuni to oxidative stress was shown to be Fur-dependent through the regulation of katA expression. Electrophoretic mobility shift assay (EMSA) demonstrated that the binding affinity between Fur and katA is reduced under low pH allowing for higher expression of katA and the defense against oxidative stress. Strikingly, the ∆fur mutant exhibited a reduced virulence capacity in both human epithelial cells and G. mellonella infection model as compared to C. jejuni wild-type. Altogether, this is the first study showing that in addition to its role in iron metabolism, Fur is an important regulator of C. jejuni acid response and cross-protection against other stresses. Moreover, our results clearly demonstrate that Fur plays a substantial role in C. jejuni host pathogenesis.

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The role of the Cj0440c gene in erythromycin-resistant (Eryr) Campylobacter jejuni

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