The Virulence Effect of CpxRA in Citrobacter rodentium Is Independent of the Auxiliary Proteins NlpE and CpxP
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PROVIDER: PRJNA472333 | ENA |
REPOSITORIES: ENA
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Project description:Citrobacter rodentium is a murine pathogen used to model the intestinal infection caused by Enteropathogenic and Enterohemorrhagic Escherichia coli (EPEC and EHEC), two diarrheal pathogens responsible for morbidity and mortality in developing and developed countries, respectively. During infection, these bacteria must sense and adapt to the gut environment of the host. In order to adapt to changing environmental cues and modulate expression of specific genes, bacteria can use two-component signal transduction systems (TCS). We have shown that the deletion of the Cpx TCS in C. rodentium leads to a marked attenuation in virulence in C3H/HeJ mice. In E. coli, the Cpx TCS is reportedly activated in response to signals from the outer-membrane lipoprotein NlpE. We therefore investigated the role of NlpE in C. rodentium virulence. We also assessed the role of the reported negative regulator of CpxRA, CpxP. We found that as opposed to the ΔcpxRA strain, neither the ΔnlpE, ΔcpxP nor the ΔnlpE/ΔcpxP strains were significantly attenuated, and had similar in vivo localization to wild-type C. rodentium. The in vitro adherence of the Cpx auxiliary protein mutants, ΔnlpE, ΔcpxP, ΔnlpEΔcpxP, was comparable to wild-type C. rodentium, whereas the ΔcpxRA strain showed significantly decreased adherence. To further elucidate the mechanisms behind the contrasting virulence phenotypes, we performed microarrays in order to define the regulon of the Cpx TCS. We detected 393 genes differentially regulated in the ΔcpxRA strain. The gene expression profile of the ΔnlpE strain is strikingly different than the profile of ΔcpxRA with regards to the genes activated by CpxRA. Further, there is no clear inverse correlation in the expression pattern of the ΔcpxP strain in comparison to ΔcpxRA. Interestingly, 161 genes were downregulated in the ΔcpxRA strain while being upregulated or unchanged in all other Cpx auxiliary protein deletion strains. This group of genes include T6SS, ompF and the regulator for colanic acid synthesis, that may contribute to the loss of virulence of ΔcpxRA. Taken together, these data suggest that in these conditions, CpxRA activates gene expression in a largely NlpE- and CpxP-independent manner.
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Project description:Identification of the targets of RegA with and without bicarbonate stimulation by comparing RegA knockout to multicopy RegA transgenics. RegA is an AraC like transcription factor identified in a mutational screen for virulence genes in Citrobacter rodentium, an attaching and effacing pathogen that causes transmissible colonic hyperplasia in mice. This experiment compares the RegA null strain with a multicopy plasmid rescue of this null strain in the presence and absence of bicarbonate with the aim of identifying pathogenesis related genes related to the early and late stages of attachment and effacement. Keywords: genetic modification, transcription factor, induction A strain of Citrobacter rodentium with a knockout of RegA was compared to the same strain rescued with a multicopy plasmid containing the wildtype RegA gene. These strains were analyzed with and without bicarbonate in an unconnected two factor design with dye balanced biological replicates.
2010-05-19 | E-GEOD-12876 | biostudies-arrayexpress
Project description:Identification of the targets of RegA with and without bicarbonate stimulation by comparing RegA knockout to multicopy RegA transgenics. RegA is an AraC like transcription factor identified in a mutational screen for virulence genes in Citrobacter rodentium, an attaching and effacing pathogen that causes transmissible colonic hyperplasia in mice. This experiment compares the RegA null strain with a multicopy plasmid rescue of this null strain in the presence and absence of bicarbonate with the aim of identifying pathogenesis related genes related to the early and late stages of attachment and effacement. Keywords: genetic modification, transcription factor, induction
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Project description:Opioids analgesics are frequently prescribed in the United States and worldwide. However, serious side effects such as addiction, immunosuppression and gastrointestinal symptoms limit their use. It has been recently demonstrated that morphine treatment results in significant disruption in gut barrier function leading to increased translocation of gut commensal bacteria. Further study indicated distinct alterations in the gut microbiome and metabolome following morphine treatment, contributing to the negative consequences associated with opioid use. However, it is unclear how opioids modulate gut homeostasis in the context of a hospital acquired bacterial infection. In the current study, a mouse model of C. rodentium infection was used to investigate the role of morphine in the modulation of gut homeostasis in the context of a hospital acquired bacterial infection. Citrobacter rodentium is a natural mouse pathogen that models intestinal infection by enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) and causes attaching and effacing lesions and colonic hyperplasia. Morphine treatment resulted in 1) the promotion of C. rodentium systemic dissemination, 2) increase in virulence factors expression with C. rodentium colonization in intestinal contents, 3) altered gut microbiome, 4) damaged integrity of gut epithelial barrier function, 5) inhibition of C. rodentium-induced increase in goblet cells, and 6) dysregulated IL-17A immune response. This is the first study to demonstrate that morphine promotes pathogen dissemination in the context of intestinal C. rodentium infection, indicating morphine modulates virulence factor-mediated adhesion of pathogenic bacteria and induces disruption of mucosal host defense during C. rodentium intestinal infection in mice. This study demonstrates and further validates a positive correlation between opioid drug use/abuse and increased risk of infections, suggesting over-prescription of opioids may increase the risk in the emergence of pathogenic strains and should be used cautiously. Therapeutics directed at maintaining gut homeostasis during opioid use may reduce the comorbidities associated with opioid use for pain management.
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Project description:Whole genome trancription study of Citrobacter rodentium grown in rich media. Publication Title: Citrobacter rodentium is an Unstable Pathogen Showing Evidence of Significant Genomic Flux Publication Author List: Nicola K. Petty, Theresa Feltwell, Derek Pickard, Simon Clare, Ana L. Toribio, Maria Fookes, Kevin Roberts, Rita Monson, Satheesh Nair, Robert A. Kingsley, Richard Bulgin, Siouxsie Wiles, David Goulding, Craig Corton, Nicola Lennard, David Harris, David Willey, Richard Rance, Lu Yu, Jyoti S. Choudhary, Carol Churcher, Michael A. Quail, Julian Parkhill, Gad Frankel, Gordon Dougan, George P.C. Salmond, Nicholas R. Thomson ArrayExpress Release Date: 2011-02-12 Person Roles: investigator Person Last Name: Thomson Person First Name: Nicholas Person Mid Initials: Person Email: nrt@sanger.ac.uk Person Phone: Person Address: Wellcome Trust Genome Campus, Hinxton, Cambridge, UK Person Affiliation: Wellcome Trust Sanger Institute Person Roles: submitter Person Last Name: Service Person First Name: Submission Person Mid Initials: Person Email: datahose@sanger.ac.uk Person Phone: Person Address: The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, CB10 1SA, United Kingdom Person Affiliation: Wellcome Trust Sanger Institute
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