Citrobacter rodentium mouse model of bacterial infection

Crepin, Valérie F.; Collins, James W.; Habibzay, Maryam; Frankel, Gad

doi:10.1038/nprot.2016.100

Cited by 82 publications

(83 citation statements)

References 83 publications

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“…S1 K). In WT mice, consistent with a previous report (Crepin et al, 2016), C. rodentium loads peaked at day 7 p.i., declined over time, and were nearly cleared after 3 wk ( Fig. 1 A).…”

Section: Rbp-j Expression In Colonic Macrophages Promotes C Rodentiusupporting

confidence: 92%

The colonic macrophage transcription factor RBP-J orchestrates intestinal immunity against bacterial pathogens

Kang

Zhang

et al. 2020

Journal of Experimental Medicine

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Macrophages play pleiotropic roles in maintaining the balance between immune tolerance and inflammatory responses in the gut. Here, we identified transcription factor RBP-J as a crucial regulator of colonic macrophage–mediated immune responses against the enteric pathogen Citrobacter rodentium. In the immune response phase, RBP-J promoted pathogen clearance by enhancing intestinal macrophage-elicited Th17 cell immune responses, which was achieved by maintenance of C/EBPβ-dependent IL-6 production by overcoming miRNA-17∼92–mediated suppressive effects. RBP-J deficiency–associated phenotypes could be genetically corrected by further deleting miRNA-17∼92 in macrophages. In the late phase, noneradicated pathogens in RBP-J KO mice recruited abundant IL-1β–expressing CD64+Ly6C+ colonic macrophages and thereby promoted persistence of ILC3-derived IL-22 to compensate for the impaired innate and adaptive immune responses, leading to ultimate clearance of pathogens. These results demonstrated that colonic macrophage–intrinsic RBP-J dynamically orchestrates intestinal immunity against pathogen infections by interfacing with key immune cells of T and innate lymphoid cell lineages.

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“…S1 K). In WT mice, consistent with a previous report (Crepin et al, 2016), C. rodentium loads peaked at day 7 p.i., declined over time, and were nearly cleared after 3 wk ( Fig. 1 A).…”

Section: Rbp-j Expression In Colonic Macrophages Promotes C Rodentiusupporting

confidence: 92%

The colonic macrophage transcription factor RBP-J orchestrates intestinal immunity against bacterial pathogens

Kang

Zhang

et al. 2020

Journal of Experimental Medicine

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“…Pathogen burden increased at 4 dpi compared with day 2 in WT mice, but the increase was dramatically and significantly greater in the Tlr9 −/− mice, with pathogen shedding numbers increasing even further at 6 dpi. C. rodentium infection is known to colonise WT mice for up to 18 days (Crepin, Collins, Habibzay, & Frankel, ). When our infected mouse strains were monitored for 18 days, both WT and Tlr9 −/− mice were able to recover from infection, with no mortality occurring during infection.…”

Section: Resultsmentioning

confidence: 99%

“…C. rodentium infection is known to colonise WT mice for up to 18 days (Crepin, Collins, Habibzay, & Frankel, 2016). When our infected mouse strains were monitored for 18 days, both WT and Tlr9 −/− mice were able to recover from infection, with no mortality occurring during infection.…”

Section: Tlr9 −/− Mice Carry Higher Intestinal Pathogen Burdensmentioning

confidence: 95%

TLR9 limits enteric antimicrobial responses and promotes microbiota‐based colonisation resistance during Citrobacter rodentium infection

Yang

Bhinder

et al. 2019

Cellular Microbiology

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Mammalian cells express an array of toll‐like receptors to detect and respond to microbial pathogens, including enteropathogenic and enterohemorrhagic Escherichia coli (EPEC and EHEC). These clinically important attaching and effacing (A/E) pathogens infect the apical surface of intestinal epithelial cells, causing inflammation as well as severe diarrheal disease. Because EPEC and EHEC are human‐specific, the related murine pathogen Citrobacter rodentium has been widely used to define how hosts defend against A/E pathogens. This study explored the role of TLR9, a receptor that recognises unmethylated CpG dinucleotides present in bacterial DNA, in promoting host defence against C. rodentium. Infected Tlr9−/− mice suffered exaggerated intestinal damage and carried significantly higher (10–100 fold) pathogen burdens in their intestinal tissues as compared with wild type (WT) mice. C. rodentium infection also induced increased antimicrobial responses, as well as hyperactivation of NF‐κB signalling in the intestines of Tlr9−/− mice. These changes were associated with accelerated depletion of the intestinal microbiota in Tlr9−/− mice as compared with WT mice. Notably, antibiotic‐based depletion of the gut microbiota in WT mice prior to infection increased their susceptibility to the levels seen in Tlr9−/− mice. Our results therefore indicate that TLR9 signalling suppresses intestinal antimicrobial responses, thereby promoting microbiota‐mediated colonisation resistance against C. rodentium infection.

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“…Moreover, virulent phages similar to CrRp3 and CrRp10 are being re-investigated as potential antimicrobial agents to both combat bacterial diseases and the dissemination of MDR bacteria (11). Because mice are resistant to EPEC and EHEC infections, C. rodentium is widely used as an in vivo model system for several important human gastrointestinal diseases (41,42). However, to the best of our knowledge, phages that infect C. rodentium have not yet been explored for antibacterial potential in preclinical animal models.…”

Section: Discussionmentioning

confidence: 99%

Isolation and characterization of bacteriophages that infect Citrobacter rodentium, a model pathogen for investigating human intestinal diseases

Luong

Cedarstrom

et al. 2018

Preprint

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Citrobacter rodentium is a mouse-restricted pathogen that has long been used as an in vivo model for two important human intestinal pathogen enteropathogenic Escherichia coli (EPEC) and enterohaemorrhagic E. coli (EHEC). And yet, in contrast to E. coli, little is known about the bacteriophages (phages) -bacterial viruses -that infect C. rodentium, reflecting in part a need to isolate and compare phages associated with this bacterial species. Here, we isolated two novel virulent phages CrRp3 and CrRp10 that infect C. rodentium and conduct in vitro and comparative genomic studies with other, related phages. We show that CrRp3 should be considered as a new species within the genus Sp6virus in the family Podoviridae, having relatively close relations to E. coli phages K1-E and K1-5 in both gene content and genome organization. By contrast, CrRp10 genome is 98% identical to that of E. coli phage Ime09 and thus should be considered as a new strain of the latter phage. We provide evidence that genomes of CrRp3 and CrRp10 have been shaped by both horizontal genetic exchange and genetic drift. Furthermore, phylogenetic analyses showed that these phages are more closely related to E. coli phages than to those infecting members of the Citrobacter genus, suggesting that CrRp3 and CrRp10 may have evolved from E. coli phages following a host-switch event.

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Citrobacter rodentium mouse model of bacterial infection

Cited by 82 publications

References 83 publications

The colonic macrophage transcription factor RBP-J orchestrates intestinal immunity against bacterial pathogens

The colonic macrophage transcription factor RBP-J orchestrates intestinal immunity against bacterial pathogens

TLR9 limits enteric antimicrobial responses and promotes microbiota‐based colonisation resistance during Citrobacter rodentium infection

Isolation and characterization of bacteriophages that infect Citrobacter rodentium, a model pathogen for investigating human intestinal diseases

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