Jian-Jun Liu1, Juan-Juan Qiu2, Xiu Shan3, Xue-Qi Shang4, Fu-Bo Sun5, Ju-Ying Jiao1,6, Ayaz Ahmed7, Yi Xin8, Dong Shang9,10,11. 1. Clinical Laboratory of Integrative Medicine, the First Affiliated Hospital of Dalian Medical University, Dalian, China. 2. Centralab, The First Affiliated Hospital of Dalian Medical University, Dalian, China. 3. Department of Oncology, the First Affiliated Hospital of Dalian Medical University, Dalian, China. 4. Department of Biotechnology, Dalian Medical University, NO.9 Western Section, Lvshun South Road, Dalian, 116044, Liaoning, China. 5. College of Medical Laboratory, Dalian Medical University, Dalian, China. 6. College of Integrative Medicine, Dalian Medical University, Dalian, 116044, China. 7. Panjwani Center for Molecular Medicine and Drug Research, University of Karachi, Karachi, Pakistan. 8. Department of Biotechnology, Dalian Medical University, NO.9 Western Section, Lvshun South Road, Dalian, 116044, Liaoning, China. jimxin@hotmail.com. 9. Clinical Laboratory of Integrative Medicine, the First Affiliated Hospital of Dalian Medical University, Dalian, China. shangdong@dmu.edu.cn. 10. College of Integrative Medicine, Dalian Medical University, Dalian, 116044, China. shangdong@dmu.edu.cn. 11. Pancreaticobiliary Centre, Department of General Surgery, the First Affiliated Hospital of Dalian Medical University, No. 222 Zhongshan Road, Dalian, 116011, Liaoning, China. shangdong@dmu.edu.cn.
Abstract
BACKGROUND/AIMS: The aim was to characterize a bacterium causing intestinal mucosal barrier damage and to identify the possible invasion mechanism. MATERIALS AND METHODS: The intestinal permeability and tight junction protein levels were detected in guinea pigs infected with Escherichia coli D-09 via immunofluorescence analysis and western blotting. In order to explain this invasion mechanism at the gene level, whole genome sequencing analysis was performed on this bacterium. RESULTS: The results showed an increased intestinal permeability and upregulated expression of the leaky protein claudin-2 in both the colon and liver of the infected animals. In addition, the draft genome of E. coli D-09 comprised 42 scaffolds (size, > 645 bp) with a total size of 4,679,567 bp. A total of 4379 protein coding genes were identified, which contained 45 antibiotic resistance and 86 virulence-related genes and covered 88.0% of the whole genome. CONCLUSIONS: This study verified that the human-derived enteroinvasive E. coli strain could destroy intestinal barrier function in guinea pigs. Additionally, our data first characterized the genome features of E. coli O124:K72 D-09, which may provide new insights into the possible invasion mechanism.
BACKGROUND/AIMS: The aim was to characterize a bacterium causing intestinal mucosal barrier damage and to identify the possible invasion mechanism. MATERIALS AND METHODS: The intestinal permeability and tight junction protein levels were detected in guinea pigs infected with Escherichia coli D-09 via immunofluorescence analysis and western blotting. In order to explain this invasion mechanism at the gene level, whole genome sequencing analysis was performed on this bacterium. RESULTS: The results showed an increased intestinal permeability and upregulated expression of the leaky protein claudin-2 in both the colon and liver of the infected animals. In addition, the draft genome of E. coli D-09 comprised 42 scaffolds (size, > 645 bp) with a total size of 4,679,567 bp. A total of 4379 protein coding genes were identified, which contained 45 antibiotic resistance and 86 virulence-related genes and covered 88.0% of the whole genome. CONCLUSIONS: This study verified that the human-derived enteroinvasive E. coli strain could destroy intestinal barrier function in guinea pigs. Additionally, our data first characterized the genome features of E. coli O124:K72 D-09, which may provide new insights into the possible invasion mechanism.
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