Citrobacter rodentium -induced colitis: A robust model to study mucosal immune responses in the gut

Koroleva, Ekaterina P.; Halperin, Sydney; Gubernatorova, Ekaterina O.; Macho-Fernandez, Elise; Spencer, Cody M.; Tumanov, Alexei V.

doi:10.1016/j.jim.2015.02.003

Cited by 50 publications

(63 citation statements)

References 91 publications

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“…However, while we observed increased relative expression of IL-23 p40 (IL-12β) subunit and no change in p19 (IL-23α) subunit; we cannot conclude on the IL-23 levels. Moreover, we did not observe increased expression of CXCL1, one of the chemokines known to recruit neutrophils to the lamina propria soon after infection (Koroleva et al, 2015), in Citrobacter dosed animals regardless of the diet, suggesting that IL-22 was upregulated via a different pathway.…”

Section: Effect Of Adr-159 On Citrobacter-induced Colitismentioning

confidence: 55%

Oral Administration of Heat-Treated Lactobacilli Modifies the Murine Microbiome and Reduces Citrobacter Induced Colitis

et al. 2020

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Significant evidence supports a relationship between the gut microbiome, inflammation, host response, and health, including the finding that a number of disorders are associated with disruption of the microbiome. In these disorders, a number of dietary interventions (including prebiotics, live probiotics, or heat-killed microbes) have been proposed to be curative or preventative agents. The use of heat-killed microbes has a number of benefits over living organisms, including reduced infection risk in vulnerable individuals, extended shelf life and the potential for use in combination with antimicrobial agents. We previously reported that murine chow supplemented with 5% ADR-159, a heat-treated fermentate generated by two Lactobacillus strains, altered both behavior and the microbiome of male mice. Now we show that ADR-159 fed female mice also display a similar microbiome shift as determined by 16S rDNA analysis. In particular, we observed a reduction of levels of Turicibacter and Clostridium sensu stricto. These subtle changes in the bacterial component of the microbiome were mirrored by changes in the virome. Extended consumption of the ADR-159 diet had no negative effect on general health and lipocalin 2 levels (LCN2; a proxy for inflammation), but we observed increased IL-17f and decreased IL-12α expression in the colon and decreased short chain fatty acid levels in the ADR-159 fed animals. Four weeks into the diet, half of the animals were dosed with Citrobacter to determine the effect of ADR-159 on infection and on pathogen induced colitis. Overall, our results suggest that while the ADR-159 diet does not prevent Citrobacter infection, it had an effect on Citrobacter-induced inflammation. In contrast to animals fed standard chow, ADR-159 fed animals did not show a reduction of small intestine length and increase of colon crypt depth, which occurred in control mice. These microbiological, histological, and immunological results provide evidence to support the impact of heat-treated microorganisms and their metabolites on the murine microbiome and health.

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Section: Effect Of Adr-159 On Citrobacter-induced Colitismentioning

confidence: 55%

Oral Administration of Heat-Treated Lactobacilli Modifies the Murine Microbiome and Reduces Citrobacter Induced Colitis

et al. 2020

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“…Citrobacter rodentium infects the murine large intestine with similar pathology to clinically important attaching and effacing Escherichia coli human pathogens (Koroleva et al, 2015). C. rodentium histologic changes and peak infection occur at 12 days following exposure to the pathogen.…”

Section: Resultsmentioning

confidence: 99%

Epithelial Histone Deacetylase 3 Instructs Intestinal Immunity by Coordinating Local Lymphocyte Activation

Navabi¹,

Whitt²,

Wu³

et al. 2017

Cell Reports

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SUMMARY Mucosal tissues are constantly in direct contact with diverse beneficial and pathogenic microbes, highlighting the need for orchestrating complex microbial signals to sustain effective host defense. Here we show an essential role for intestinal epithelial cell expression of histone deacetylase 3 (HDAC3) in responding to pathogenic microbes and activating protective innate immunity. Mice lacking HDAC3 in intestinal epithelial cells were more susceptible to Citrobacter rodentium when under tonic stimulation by the commensal microbiota. This impaired host defense reflected significantly decreased IFNγ production by intraepithelial CD8+ T cells early during infection. Further, HDAC3 was necessary for infection-induced epithelial expression of the IFNγ-inducing factor IL-18 and administration of IL-18 restored IFNγ activity to resident CD8+ T cells and reduced infection. Thus, HDAC3 mediates communication between intestinal epithelial cells and resident lymphocytes, revealing that epithelial priming by an epigenetic modifier may direct mucosal regulation of host defense against pathogenic microbes.

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“…Thus, the accumulation of PFOS in the intestine may have deleterious effect on intestinal diseases, such as intestinal infection, intestinal autoimmune diseases and tumor. In this study, we determined the effect of PFOS on intestinal immunity and intestinal infection using a mouse model of Citrobacter rodentium infection, which recapitulates human enteropathogenic E. coli and enterohemorrhagic E. coli infection 17–19 . We have found PFOS affects the outcome of C. rodentium infection through modulating intestinal immunity and microbiota.…”

Section: Discussionmentioning

confidence: 99%

“…Mouse Citrobacter rodentium infection has been widely used as a model for studying human intestinal infections, such as enteropathogenic E. coli and enterohemorrhagic E. coli infection 17–19 . Innate and adaptive immune cells are activated by antigens derived from C. rodentium and exhibit immune defensive function to clear the pathogen.…”

Section: Introductionmentioning

confidence: 99%

Perfluorooctane sulfonate affects intestinal immunity against bacterial infection

Suo

Fan

Zhou

et al. 2017

Sci Rep

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Perfluorooctane sulfonate (PFOS) is an environmental contaminant that has been manufactured to be used as surfactants and repellents in industry. Due to long half-life for clearance and degradation, PFOS is accumulative in human body and has potential threat to human health. Previous studies have shown the development and function of immune cells can be affected by PFOS. Although PFOS has a high chance of being absorbed through the oral route, whether and how PFOS affects immune cells in the gut is unknown. Using mouse model of Citrobacter rodentium infection, we investigated the role of PFOS on intestinal immunity. We found at early phase of the infection, PFOS inhibited the expansion of the pathogen by promoting IL-22 production from the group 3 innate lymphoid cell (ILC3) in an aryl hydrocarbon receptor dependent manner. Nevertheless, persistent PFOS treatment in mice finally led to a failure to clear the pathogen completely. At late phase of infection, enhanced bacterial counts in PFOS treated mice were accompanied by increased inflammatory cytokines, reduced mucin production and dysbiosis, featured by decreased level of Lactobacillus casei, Lactobacillus johnsonii and increased E. coli. Our study reveals a deleterious consequence in intestinal bacterial infection caused by PFOS accumulation.

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Citrobacter rodentium -induced colitis: A robust model to study mucosal immune responses in the gut

Cited by 50 publications

References 91 publications

Oral Administration of Heat-Treated Lactobacilli Modifies the Murine Microbiome and Reduces Citrobacter Induced Colitis

Oral Administration of Heat-Treated Lactobacilli Modifies the Murine Microbiome and Reduces Citrobacter Induced Colitis

Epithelial Histone Deacetylase 3 Instructs Intestinal Immunity by Coordinating Local Lymphocyte Activation

Perfluorooctane sulfonate affects intestinal immunity against bacterial infection

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