作者: Kiran Palyada , Yi-Qian Sun , Annika Flint , James Butcher , Hemant Naikare
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摘要: During gut colonization, the enteric pathogen Campylobacter jejuni must surmount toxic effects of reactive oxygen species produced by its own metabolism, host immune system, and intestinal microflora. Elucidation C. oxidative stress defense mechanisms is critical for understanding pathophysiology. The in were characterized transcriptional profiling phenotypic analysis wild-type mutant strains. To define regulon peroxide-sensing regulator, PerR, we constructed an isogenic ΔperR compared transcriptome profile with that strain. Transcriptome identified 104 genes belonged to PerR regulon. appears regulate gene expression a manner both depends on independent presence iron and/or H2O2. Mutation perR significantly reduced motility. A using chick colonization model showed exhibited attenuated behavior. An changes induced exposure H2O2, cumene hydroperoxide, or menadione revealed differential belonging variety biological pathways, including classical systems, heat shock response, DNA repair fatty acid biosynthesis, multidrug efflux pumps. Mutagenic studies superoxide dismutase SodB, alkyl-hydroxyperoxidase AhpC, catalase KatA, role these proteins colonization. This study reveals interplay between Fur, metabolism defense, highlights elements cecum subsequent survival.