Communicable Ulcerative Colitis Induced by T-bet Deficiency in the Innate Immune System

Garrett, Wendy S.; Lord, Graham M.; Punit, Shivesh; Lugo-Villarino, Geanncarlo; Mazmanian, Sarkis K.; Ito, Susumu; Glickman, Jonathan N.; Glimcher, Laurie H.

doi:10.1016/j.cell.2007.08.017

Cited by 843 publications

(797 citation statements)

References 37 publications

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“…In several disease models, microbial transfer of intestinal disease can be accomplished by housing healthy WT mice with colitic mice (Garrett et al, 2007;Elinav et al, 2011). Mice are coprophagic, and sharing the microbial community in this manner presumably has a substantial effect on maintenance of microbial community structure.…”

Section: Discussionmentioning

confidence: 99%

Stochastic changes over time and not founder effects drive cage effects in microbial community assembly in a mouse model

et al. 2013

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Maternal transmission and cage effects are powerful confounding factors in microbiome studies. To assess the consequences of cage microenvironment on the mouse gut microbiome, two groups of germ-free (GF) wild-type (WT) mice, one gavaged with a microbiota harvested from adult WT mice and another allowed to acquire the microbiome from the cage microenvironment, were monitored using Illumina 16S rRNA sequencing over a period of 8 weeks. Our results revealed that cage effects in WT mice moved from GF to specific pathogen free (SPF) conditions take several weeks to develop and are not eliminated by the initial gavage treatment. Initial gavage influenced, but did not eliminate a successional pattern in which Proteobacteria became less abundant over time. An analysis in which 16S rRNA sequences are mapped to the closest sequenced whole genome suggests that the functional potential of microbial genomes changes significantly over time shifting from an emphasis on pathogenesis and motility early in community assembly to metabolic processes at later time points. Functionally, mice allowed to naturally acquire a microbial community from their cage, but not mice gavaged with a common biome, exhibit a cage effect in Dextran Sulfate Sodium-induced inflammation. Our results argue that while there are long-term effects of the founding community, these effects are mitigated by cage microenvironment and successional community assembly over time, which must both be explicitly considered in the interpretation of microbiome mouse experiments.

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Section: Discussionmentioning

confidence: 99%

Stochastic changes over time and not founder effects drive cage effects in microbial community assembly in a mouse model

et al. 2013

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“…Mice that are deficient in the transcription factor T-bet develop colitis. T-bet defines T-cells of the T-helper 1 subset, which are proinflammatory T-helper cells that are important in the clearance of viral and other intracellular infections and typically secrete the cytokine interferon-g. By transferring the colonic flora from mice with T-bet deficiency and colitis to wild-type animals the colitis can be transferred too, suggesting that the flora has become 'colitogenic' (17) .…”

Section: What Is the Microbiome?mentioning

confidence: 99%

Nutrition, intestinal defence and the microbiome

Kelly

2010

Proc. Nutr. Soc.

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The interaction between nutrition and infection was the subject of important work by several groups in the 1960s. The explosion of knowledge in immunology, including innate immunity, has led to increased understanding of the impact of nutrition on host defence, but much more work needs to be done in this area. In the last decade an increasing volume of work has opened up the previously obscure world of human endogenous flora. This work suggests that the microbiome, the total genetic pool of the microbiota, contributes to the already complex interaction between nutrition and infectious disease. The established concept that nutritional status, host defence and infection all impact on each other now has to be expanded into a multiple interaction, with the microbiota interacting with all three other elements. There is good evidence that the microbiome programmes host defence and drives a metabolome that impacts on energy balance, and indeed on some micronutrients. In turn, host defence shapes the microbiome, and nutritional status, particularly micronutrient status, helps determine several elements of host defence. While interventions in this area are in their infancy, the understanding of interactions that already have an enormous impact on global health is now at a threshold. The present review explores the evidence for these interactions with a view to putting potential interventions into the context of a conceptual framework.

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“…2 While there is a paucity of human data evaluating the risks of such unfavorable changes, animal studies suggest that in genetically predisposed germ-free mice, transfer of dysbiotic microbiota can induce terminal ileitis or colitis. [3][4][5] We report a novel case-series of patients who received FMT for recurrent Clostridium difficile infections from a donor who was later diagnosed with ileocolonic Crohn's disease. Between August and December 2013, 31 patients received FMT by colonoscopy for treatment of non-responsive C. difficile from this single, unrelated, on-site donor at an academic center.…”

Section: To the Editormentioning

confidence: 99%

Can you cause inflammatory bowel disease with fecal transplantation? A 31-patient case-series of fecal transplantation using stool from a donor who later developed Crohn's disease

et al. 2017

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Communicable Ulcerative Colitis Induced by T-bet Deficiency in the Innate Immune System

Cited by 843 publications

References 37 publications

Stochastic changes over time and not founder effects drive cage effects in microbial community assembly in a mouse model

Stochastic changes over time and not founder effects drive cage effects in microbial community assembly in a mouse model

Nutrition, intestinal defence and the microbiome

Can you cause inflammatory bowel disease with fecal transplantation? A 31-patient case-series of fecal transplantation using stool from a donor who later developed Crohn's disease

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