ArticleFrontiers in cellular and infection microbiology2024
Pathogenicity and identification of host adaptation genes of the avian pathogenic
Article in Frontiers in cellular and infection microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Molecular epidemiology and pathogenic potential ofFrontiers in microbiology · 2026Article
- Molecular epidemiology ofFrontiers in microbiology · 2026Article
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11 authors.
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Abstract
Introduction: Avian pathogenic Methods: A virulent strain, NC22, was selected to elucidate the mechanisms underlying APEC O145-related pathogenicity and host adaptation. Whole-genome sequencing and pathogenicity assays was conducted on this strain. We further performed a transcriptional analysis of the bacteria during the early colonization stage in the duck liver and compared them with those in liquid cultures Results: Subcutaneous inoculation of NC22 induced typical symptoms in ducks. The bacterial loads in the blood and various tissues peaked at 2 and 3 days post infection, respectively. The affected tissues included the heart, liver, spleen, lung, kidney, bursa of Fabricius, duodenum, jejunum, and cecum. We then analyzed the transcriptome profiles of NC22 during growth in duck liver versus lysogeny broth and identified 87 genes with differential expression levels.These included key metabolic enzymes and recognized host adaptation factors. Analysis of the metabolic pathways revealed an inhibition of the metabolic shift from glycolysis towards pentose phosphate pathway and an interference of the citrate cycle. Moreover, significantly differentially expressed small regulatory RNAs were examined, such as SroC, CsrC, and GadY. Discussion: These findings enhance our understanding of the pathogenicity of APEC O145 and the molecular mechanisms underlying APEC-related pathogen-host interactions.
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