Long-term Selenium Deficiency Increases the Pathogenicity of a Citrobacter rodentium Infection in Mice

Smith, Allen; Cheung, Lumei; Botero, Sebastian

doi:10.1007/s12011-011-9071-4

Cited by 16 publications

(14 citation statements)

References 70 publications

(90 reference statements)

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“…Increased susceptibility to infections, such as Escherichia coli , is attributed to peripheral immune suppression as a direct consequence of CNS injury, not only during hospitalizations, but also long term 19–21 . Citrobacter rodentium (Cr) infection is a murine model for human enterohemorrhoragic E. coli and enteropathogenic E. coli infection, and has a well-characterized immune response with defined pathological hallmarks 22 .…”

Section: Introductionmentioning

confidence: 99%

Bidirectional brain-gut interactions and chronic pathological changes after traumatic brain injury in mice

Elise

Smith

Desai

et al. 2017

Brain, Behavior, and Immunity

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123

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Objectives Traumatic brain injury (TBI) has complex effects on the gastrointestinal tract that are associated with TBI-related morbidity and mortality. We examined changes in mucosal barrier properties and enteric glial cell response in the gut after experimental TBI in mice, as well as effects of the enteric pathogen Citrobacter rodentium (Cr) on both gut and brain after injury. Methods Moderate-level TBI was induced in C57BL/6 mice by controlled cortical impact (CCI). Mucosal barrier function was assessed by transepithelial resistance, fluorescent-labelled dextran flux, and quantification of tight junction proteins. Enteric glial cell number and activation were measured by Sox10 expression and GFAP reactivity, respectively. Separate groups of mice were challenged with Cr infection during the chronic phase of TBI, and host immune response, barrier integrity, enteric glial cell reactivity, and progression of brain injury and inflammation were assessed. Results Chronic CCI induced changes in colon morphology, including increased mucosal depth and smooth muscle thickening. At day 28 post-CCI, increased paracellular permeability and decreased claudin-1 mRNA and protein expression were observed in the absence of inflammation in the colon. Colonic glial cell GFAP and Sox10 expression were significantly increased 28 days after brain injury. Clearance of Cr and upregulation of Th1/Th17 cytokines in the colon were unaffected by CCI; however, colonic paracellular flux and enteric glial cell GFAP expression were significantly increased. Importantly, Cr infection in chronically-injured mice worsened the brain lesion injury and increased astrocyte- and microglial-mediated inflammation. Conclusion These experimental studies demonstrate chronic and bidirectional brain-gut interactions after TBI, which may negatively impact late outcomes after brain injury.

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Section: Introductionmentioning

confidence: 99%

Bidirectional brain-gut interactions and chronic pathological changes after traumatic brain injury in mice

Elise

Smith

Desai

et al. 2017

Brain, Behavior, and Immunity

Self Cite

123

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“…Perhaps it is expected that GPx1 and GPx2 play a important role in defending bacterial infection, because expression of both Gpx1 and Gpx2 is modulated by selenium (Se) [5] and Se-deficient mice were susceptible to food borne pathogens such as Listeria monocytogenes and Citrobacter rodentium [40–42]. Nevertheless, this is the first report to identify GPx1 and GPx2 as two major selenoproteins that protect gut from bacteria-induced colitis.…”

Section: Discussionmentioning

confidence: 99%

The Gdac1 locus modifies spontaneous and Salmonella-induced colitis in mice deficient in either Gpx2 or Gpx1 gene

Esworthy

Kim

Wang

et al. 2013

Free Radical Biology and Medicine

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We previously identified a Gdac1 (Gpx-deficiency-associated colitis 1) locus that influences the severity of spontaneous colitis in Gpx1- and Gpx2-double knockout (Gpx1/2-DKO) mice. Congenic Gpx1/2-DKO mice in the129S1/SvImJ (129) background but carrying the Gdac1B6 allele have milder spontaneous colitis than 129 Gpx1/2-DKO mice carrying the Gdac1129 allele. Here, we evaluated the effect of the Gdac1B6 allele on 129 strain non-DKO mice that had a wild-type (WT) Gpx1 or Gpx2 allele and WT mice. We found the congenic Gdac1B6 Gpx2-KO, Gpx1-KO and WT mice also had better health than the corresponding 129 mice measured by at least one of the parameters including disease signs, colon length or weight gain. The Gdac1B6 allele prevented loss of goblet cells and crypt epithelium exfoliation in the Gpx1/2-DKO mice, but did not affect epithelial cell apoptosis or proliferation. Because Gdac1B6 affects gut dysbiosis in the DKO mice, we then tested its impact on bacteria-induced colitis in non-DKO mice. First, we found both Gpx1-KO and Gpx2-KO mice were susceptible to Salmonella enterica serotype Typhimurium (S. Tm)-induced colitis under conditions where WT B6 and 129 mice were resistant. Second, the S. Tm-infected Gdac1B6 Gpx1-KO mice had stronger inflammatory responses than 129 Gpx1-KO, 129 Gpx2-KO with both Gdac1 allele and WT mice by having higher mRNA levels of Nod2, Nox2, Tnf and Cox2. We conclude that the Gdac1 locus affects both spontaneous and S. Tm-induced colitis in 129 non-DKO mice although in opposite directions.

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“…Mice were infected with Cr using established protocols [ 26 , 30 , 31 ]. The Cr strain used in this study was a nalidixic acid-resistant mutant of strain DBS100 (ATCC 51459).…”

Section: Methodsmentioning

confidence: 99%

Dietary Indole-3-Carbinol Alleviated Spleen Enlargement, Enhanced IgG Response in C3H/HeN Mice Infected with Citrobacter rodentium

Wang

et al. 2020

Nutrients

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Enteropathogenic and enterohemorrhagic Escherichia coli are important enteric pathogens that induce hemorrhagic colitis or even fatal hemolytic uremic syndrome. Emerging evidence shows that some bio-actives derived from fruits and vegetables may serve as alternatives to antibiotics for overcoming multidrug resistant E. coli infections. In this study, the Citrobacter rodentium (Cr) infection model was utilized to mimic E. coli-induced acute intestinal inflammation, and the effects of a cruciferous vegetable-derived cancer protective compound, indole-3-carbinol (I3C), on the immune responses of Cr-susceptible C3H/HeN mice were investigated. Dietary I3C significantly inhibited the loss of body weight and the increase in spleen size in Cr infected mice. In addition, I3C treatment reduced the inflammatory response to Cr infection by maintaining anti-inflammatory cytokine IL-22 mRNA levels while reducing expression of other pro-inflammatory cytokines including IL17A, IL6, IL1β, TNF-α, and IFN-γ. Moreover, the serum cytokine levels of IL17, TNF-α, IL12p70, and G-CSF also were down-regulated by I3C in Cr-infected mice. Additionally, dietary I3C specifically enhanced the Cr-specific IgG response to Cr infection. In general, dietary I3C reduced the Cr-induced pro-inflammatory response in susceptible C3H/HeN mice and alleviated the physiological changes and tissue damage induced by Cr infection but not Cr colonization.

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Long-term Selenium Deficiency Increases the Pathogenicity of a Citrobacter rodentium Infection in Mice

Cited by 16 publications

References 70 publications

Bidirectional brain-gut interactions and chronic pathological changes after traumatic brain injury in mice

Bidirectional brain-gut interactions and chronic pathological changes after traumatic brain injury in mice

The Gdac1 locus modifies spontaneous and Salmonella-induced colitis in mice deficient in either Gpx2 or Gpx1 gene

Dietary Indole-3-Carbinol Alleviated Spleen Enlargement, Enhanced IgG Response in C3H/HeN Mice Infected with Citrobacter rodentium

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