The Pathogenicity of an Enteric<i>Citrobacter rodentium</i>Infection Is Enhanced by Deficiencies in the Antioxidants Selenium and Vitamin E

Smith, Allen; Botero, Sebastian; Shea‐Donohue, Terez; Urban, Joseph F.

doi:10.1128/iai.01017-10

Cited by 44 publications

(36 citation statements)

References 60 publications

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“…Increased pathology was accompanied by a large increase in infiltrating cells that correlated with increased expression of several members of the CXCL chemokine family as well as CCL2. These results are very similar to those obtained with mice fed a selenium-and vitamin E double-deficient diet for 6 weeks [27]. It is known that vitamin E deficiency exacerbates selenium deficiency [41], and this may account for the similar results obtained in a shorter timeframe in mice fed a diet deficient in both selenium and vitamin E.…”

Section: Discussionsupporting

confidence: 92%

“…Our previous work established that deficiencies in selenium altered the clearance of a gastrointestinal nematode parasite, Heligmosomoides polygyrus, from mice [25,26]. Furthermore, a double deficiency in selenium and vitamin E resulted in increased pathology in response to infection of mice with C. rodenitum [27]. Here, we provide evidence that selenium is critical for optimal resistance and reduced pathogenicity to infection with C. rodentium.…”

Section: Introductionmentioning

confidence: 59%

“…Previous work established that mice fed a diet-deficient in selenium and vitamin E for 6 weeks prior to infection with C. rodentium had increased pathology [27]. The aim of the current study was to examine the effect of feeding mice diets deficient in only selenium for either 5 or 20 weeks on the response to infection with C. rodentium.…”

Section: Discussionmentioning

confidence: 98%

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

Smith

Cheung

Botero

2011

Biol Trace Elem Res

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Citrobacter rodentium is a mouse pathogen that causes infectious colitis and shares characteristics with human enteropathogenic (EPEC) and enterohemorrhagic (EHEC) Escherichia coli, including the ability to cause attaching and effacing lesions in the colon and serves as a useful model to study the pathogenicity of these bacteria. In this study, mice were fed a selenium-deficient diet for 5 or 20 weeks and then infected with C. rodentium. Colonization of the colon by C. rodentium was similar in mice fed adequate or selenium-deficient diets, but total bacterial colonization of the spleen was elevated in mice fed selenium-deficient diet for 20 weeks. Infection-induced changes to the colon included inflammatory cell infiltration, gross changes in crypt architecture, and ulceration and denuding of the epithelial layer that were greatest in mice fed a selenium-deficient diet for 20 weeks. Expression of pro-inflammatory genes was significantly higher 12-days post-infection in mice fed the selenium-deficient diet for 20 weeks compared to mice fed a selenium-adequate diet or selenium-deficient diet for 5 weeks. Diarrhea was prevalent in mice fed the selenium-deficient diet for 20 weeks but not 5 weeks, and this was associated with decreased expression of solute carrier family 26a3 and carbonic anhydrase IV, genes involved in ion transport. These results indicated that selenium played an important role in resistance to the pathological effects of a C. rodentium infection, and therefore, selenium status may be important in the expression of human disease caused by common food-borne bacteria.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 59%

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

Smith

Cheung

Botero

2011

Biol Trace Elem Res

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“…Interestingly, this increased neutrophil influx was also associated with upregulated expression of the genes for the innate immune response-related cytokines IL-1␤, iNOS, IL-17a, IL-6, and TNF-␣ at day 14 p.i. In agreement with previous reports, we found that the expression of the genes for these innate immune cytokines was higher in infected, vehicle-treated mice than in noninfected controls at peak infection (22,48). These cytokines play a significant role in host defense and clearance of C. rodentium early during infection (13,20,25,53).…”

Section: Discussionsupporting

confidence: 81%

The Sphingosine-1-Phosphate Analogue FTY720 Impairs Mucosal Immunity and Clearance of the Enteric Pathogen Citrobacter rodentium

et al. 2012

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The sphingosine-1-phosphate (S1P) analogue FTY720 is therapeutically efficacious in multiple sclerosis and in the prevention of transplant rejection. It prevents the migration of lymphocytes to sites of pathology by trapping them within the peripheral lymph nodes, mesenteric lymph nodes (MLNs), and Peyer's patches. However, evidence suggests that its clinical use may increase the risk of mucosal infections. We investigated the impact of FTY720 treatment on susceptibility to gastrointestinal infection with the mouse enteric pathogen Citrobacter rodentium. This attaching and effacing bacterium induces a transient bacterial colitis in immunocompetent mice that resembles human infection with pathogenic Escherichia coli. FTY720 treatment induced peripheral blood lymphopenia, trapped lymphocytes in the MLNs, and prevented the clearance of bacteria when mice were infected with luciferase-tagged C. rodentium. FTY720-treated C. rodentium-infected mice had enhanced colonic inflammation, with significantly higher colon mass, colon histopathology, and neutrophil infiltration than vehicle-infected animals. In addition, FTY720-treated infected mice had significantly lower numbers of colonic dendritic cells, macrophages, and T cells. Gene expression analysis demonstrated that FTY720-treated infected mice had an impaired innate immune response and a blunted mucosal adaptive immune response, including Th1 cytokines. The data demonstrate that the S1P analogue FTY720 adversely affects the immune response to and clearance of C. rodentium.

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“…Sedeficiency has been shown to exacerbate infection of mice with Citrobacter rodentium, which shares many characteristics with human enteropathogenic (EPEC13) and enterohemorrhagic E. coli (EHEC) (233). Infections with this pathogen in mice produce robust immune responses characterized by a mixed Th1/Th17 response (100,114).…”

Section: Intestinal Inflammation and Food-borne Illnessesmentioning

confidence: 99%

The Role of Selenium in Inflammation and Immunity: From Molecular Mechanisms to Therapeutic Opportunities

Huang

Rose

Hoffmann

2012

Antioxidants & Redox Signaling

716

496

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Dietary selenium (]Se), mainly through its incorporation into selenoproteins, plays an important role in inflammation and immunity. Adequate levels of Se are important for initiating immunity, but they are also involved in regulating excessive immune responses and chronic inflammation. Evidence has emerged regarding roles for individual selenoproteins in regulating inflammation and immunity, and this has provided important insight into mechanisms by which Se influences these processes. Se deficiency has long been recognized to negatively impact immune cells during activation, differentiation, and proliferation. This is related to increased oxidative stress, but additional functions such as protein folding and calcium flux may also be impaired in immune cells under Se deficient conditions. Supplementing diets with above-adequate levels of Se can also impinge on immune cell function, with some types of inflammation and immunity particularly affected and sexually dimorphic effects of Se levels in some cases. In this comprehensivearticle, the roles of Se and individual selenoproteins in regulating immune cell signaling and function are discussed. Particular emphasis is given to how Se and selenoproteins are linked to redox signaling, oxidative burst, calcium flux, and the subsequent effector functions of immune cells. Data obtained from cell culture and animal models are reviewed and compared with those involving human physiology and pathophysiology, including the effects of Se levels on inflammatory or immune-related diseases including anti-viral immunity, autoimmunity, sepsis, allergic asthma, and chronic inflammatory disorders. Finally, the benefits and potential adverse effects of intervention with Se supplementation for various inflammatory or immune disorders are discussed. Antioxid. Redox Signal. 16, 705-743.

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The Pathogenicity of an EntericCitrobacter rodentiumInfection Is Enhanced by Deficiencies in the Antioxidants Selenium and Vitamin E

Cited by 44 publications

References 60 publications

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

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

The Sphingosine-1-Phosphate Analogue FTY720 Impairs Mucosal Immunity and Clearance of the Enteric Pathogen Citrobacter rodentium

The Role of Selenium in Inflammation and Immunity: From Molecular Mechanisms to Therapeutic Opportunities

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