Intestinal Microbiota in Animal Models of Inflammatory Diseases

Hörmannsperger, Gabriele; Schaubeck, Monika; Haller, Dirk

doi:10.1093/ilar/ilv019

Cited by 39 publications

(29 citation statements)

References 111 publications

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“…This finding is supported further by studies in SAMP1/YitFc mice showing dysfunction within their mesenteric lymph node regulatory T-cell compartment 74 . Studies performed in Tnf ΔARE/+ mice also confirm the importance of host-gut microbiome interactions and dysbiosis in the pathogenesis of CD-like ileitis 75, 76. Schaubeck et al 77 recently showed that germ-free Tnf ΔARE/ + mice were free of intestinal inflammation.…”

Section: Pathogenic Mechanisms Of Crohn’s-like Ileitismentioning

confidence: 79%

Uncovering Pathogenic Mechanisms of Inflammatory Bowel Disease Using Mouse Models of Crohn’s Disease–Like Ileitis: What is the Right Model?

Cominelli

Arseneau

Rodriguez-Palacios

et al. 2017

Cellular and Molecular Gastroenterology and Hepatology

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Crohn’s disease and ulcerative colitis, together known as inflammatory bowel disease, are debilitating chronic disorders of unknown cause and cure. Our evolving understanding of these pathologies is enhanced greatly by the use of animal models of intestinal inflammation that allow in vivo mechanistic studies, preclinical evaluation of new therapies, and investigation into the causative factors that underlie disease pathogenesis. Several animal models, most commonly generated in mice, exist for the study of colitis. The appropriateness of their use often can be determined by their mode of generation (ie, chemical induction, T-cell transfer, targeted genetic manipulation, spontaneously occurring, and so forth), the type of investigation (mechanistic studies, pathogenic experiments, preclinical evaluations, and so forth), and the type of inflammation that occurs in the model (acute vs chronic colitis, tissue injury/repair, and so forth). Although most murine models of inflammatory bowel disease develop inflammation in the colon, Crohn’s disease most commonly occurs in the terminal ileum, where a very limited number of mouse models manifest disease. This review discusses appropriate experimental applications for different mouse models of colitis, and highlights the particular utility of 2 highly relevant models of Crohn’s-like ileitis—the spontaneous SAMP1/YitFc inbred mouse strain and the genetically engineered TnfΔAU-rich element/+ mouse model of tumor necrosis factor overexpression, both of which bear strong resemblance to the human condition. Similar to patients with Crohn’s disease, SAMP1/YitFc ileitis develops spontaneously, without chemical, genetic, or immunologic manipulation, making this model particularly relevant for studies aimed at identifying the primary defect underlying the occurrence of Crohn’s ileitis, as well as preclinical testing of novel treatment modalities.

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Section: Pathogenic Mechanisms Of Crohn’s-like Ileitismentioning

confidence: 79%

Uncovering Pathogenic Mechanisms of Inflammatory Bowel Disease Using Mouse Models of Crohn’s Disease–Like Ileitis: What is the Right Model?

Cominelli

Arseneau

Rodriguez-Palacios

et al. 2017

Cellular and Molecular Gastroenterology and Hepatology

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“…Correlation analysis revealed that the ileal expression of Il1β was positively correlated to the Bacteroides genus although this genus was not significantly affected by the dietary treatments. The usual limitations linked to individual experimental animals also apply to this study 47 . Only one gender and one genetic background were tested.…”

Section: Discussionmentioning

confidence: 99%

Fat binding capacity and modulation of the gut microbiota both determine the effect of wheat bran fractions on adiposity

Suriano

Bindels

Verspreet

et al. 2017

Sci Rep

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The aim of this study was to determine the impact of different wheat bran fractions on the gut microbiota and fat binding capacity to explain their differential effects on metabolic and inflammatory disorders induced by a western diet (WD) in mice. Wheat bran derived arabinoxylan oligosaccharides (AXOS), a crude fraction of wheat bran (WB), or the same wheat bran with reduced particle size (WBs) were added to the WD of mice for 8 weeks. AXOS shifted the gut microbiota composition, blunted Clostridium and Turicibacter genera and strongly promoted Bifidobacterium and Butyricicoccus genera, independently of changes in gut antimicrobial peptide expression. AXOS was the most efficient to reduce adiposity. Only WB fraction promoted fat excretion and differed from the other fractions by the capacity to increase the Akkermansia genus and to counteract gut interleukin 1 beta (IL1β) overexpression. Strikingly, WBs promoted steatosis and adipose tissue inflammation, despite its ability -like WB- to increase bacterial diversity. In conclusion, wheat bran fractions differently affect metabolic and inflammatory disorders associated with WD feeding, depending on their particle size, their fat binding capacity and their influence on the gut microbiota. Those results might be useful to take into account in nutritional advices to control obesity.

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“…Gnotobiotic models have been used to reveal causative association between changes in the microbiome in health and disease and to gain functional insights into host-microbe interactions. 77 To address this aspect, a reductionist approach has been adopted to focus the investigation on specific taxa or metabolites of interest, revealing the potential mechanism or mechanisms responsible for the phenomenon observed. One example is the use of IBD-related mouse models monoassociated with a variety of commensal bacteria, including Escherichia coli, Enterococcus faecalis, Bacteroides vulgatus, and Bilophila wadsworthia.…”

Section: Gnotobiotic Model Systems: From Single-strain To Bacterial Cmentioning

confidence: 99%

Functional relevance of microbiome signatures: The correlation era requires tools for consolidation

Buttó

Haller

2017

Journal of Allergy and Clinical Immunology

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Compelling research over the past decade identified a fundamental role of the intestinal microbiome on human health. Compositional and functional changes of this microbial ecosystem are correlated with a variety of human pathologies. Metagenomic resolution and bioinformatic tools considerably improved, allowing even strain-level analysis. However, the search for microbial risk patterns in human cohorts is often confounded by environmental factors (eg, medication) and host status (eg, disease relapse), questioning the prognostic and therapeutic value of the currently available information. In addition to a better stratification of human phenotypes, the implementation of standardized protocols for sampling and analysis is needed to improve the reproducibility and comparability of microbiome signatures at a meaningful taxonomic resolution. At the level of mechanistic understanding, the molecular integration of pleiotropic signals coming from this complex and dynamically changing ecosystem is one of the biggest challenges in this field. The first successful attempts to apply reverse genetics based on the available metagenomic information yielded identification of small molecules and metabolites with functional relevance for microbe-host interactions. Further expansion on the isolation of bacteria from the "unculturable biomass" will help characterize microbiome signatures in model systems, finally aiming at the development of clinically relevant synthetic consortia with safe and functionally well-defined strains. In conclusion and beyond reasonable enthusiasm, the mechanistic implementation and clinical relevance of microbiome alterations on disease susceptibility is still in its infancy, but the integration of all the above-mentioned strategies will help overcome the correlation era in microbiome research and lead to a rational evaluation of clinical strategies relevant for targeted microbial intervention.

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Intestinal Microbiota in Animal Models of Inflammatory Diseases

Cited by 39 publications

References 111 publications

Uncovering Pathogenic Mechanisms of Inflammatory Bowel Disease Using Mouse Models of Crohn’s Disease–Like Ileitis: What is the Right Model?

Uncovering Pathogenic Mechanisms of Inflammatory Bowel Disease Using Mouse Models of Crohn’s Disease–Like Ileitis: What is the Right Model?

Fat binding capacity and modulation of the gut microbiota both determine the effect of wheat bran fractions on adiposity

Functional relevance of microbiome signatures: The correlation era requires tools for consolidation

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