Perturbation of the Human Microbiome as a Contributor to Inflammatory Bowel Disease

Missaghi, Bayan; Barkema, Herman W.; Madsen, Karen; Ghosh, Subrata

doi:10.3390/pathogens3030510

Cited by 30 publications

(23 citation statements)

References 109 publications

(146 reference statements)

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“…Recent murine studies have identified that functional microbial pathway alterations can be induced by sub-therapeutic administration of antibiotics as well. This evidence supports the idea that antibiotic therapy in IBD may reverse or improve the existing dysbiosis [5] .…”

Section: Ibd-associated Microbiome Changes Relative To Antibody Therapysupporting

confidence: 83%

“…A dominant characteristic of patients with IBD is intestinal dysbiosis, a reduction in the diversity of bacterial species overall and especially in the number of beneficial microbes, such as Firmicutes (e.g., Faecalibacterium prausnitzii and Roseburia ), and an increase in enteric pathogens, such as adherent invasive E. coli and other Enterobacteriaceae [5] . The shift in bacterial species highlights the metabolic transition of the microbiome ecosystem from facultative to obligate anaerobes.…”

Section: The Gut Microbiome and Ibdmentioning

confidence: 99%

“…Typically, the gut microbial ecology matures around 3 years of age and then remains stable until late adulthood [5] . Studies of this nature have been limited by the abundant variations of both microbe species and populations between individuals attributed to differences in diet, proximal exposure to animals and humans, travel, environments and smoking [13] .…”

Section: The Gut Microbiome and Ibdmentioning

confidence: 99%

“…Initial supporting evidence is provided from the North American livestock community. Since the 1950s, widespread sub-therapeutic administration of antibiotics has increased animal growth up to 15% [5] . Human studies have identified that antibiotic use within the first year of life alters the microbiome thereby increasing the risk of future autoimmune dis-ease.…”

Section: Ibd-associated Microbiome Changes Relative To Antibody Therapymentioning

confidence: 99%

“…[4] . Another microbe-oriented feature is that patients with IBD have a substantial decrease in the diversity of their intestinal microbiota [5] . Whether this dysbiosis is a cause or consequence of another primary event remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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Practical Considerations and the Intestinal Microbiome in Disease: Antibiotics for IBD Therapy

Fedorak

Ismond²

2016

Dig Dis

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The inflammatory bowel diseases, Crohn's and ulcerative colitis, have been treated with a range of antibiotics for inducing and maintaining remission, as well as the prevention of post-operative symptoms. To date, many studies have been performed assessing the efficacy of antibiotics when used alone, in combination with other antibiotics, or as an adjunctive therapy to other pharmaceutical treatments. Literature evidence supporting the use of antibiotics in IBD can be ambiguous, especially when considering the potential role of dysbiosis in the gastrointestinal tract. The review considers the systemic effect of antibiotics and the evidence base for their efficacy in the treatment of IBD.

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Section: Ibd-associated Microbiome Changes Relative To Antibody Therapysupporting

confidence: 83%

Section: The Gut Microbiome and Ibdmentioning

confidence: 99%

Section: The Gut Microbiome and Ibdmentioning

confidence: 99%

Section: Ibd-associated Microbiome Changes Relative To Antibody Therapymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Practical Considerations and the Intestinal Microbiome in Disease: Antibiotics for IBD Therapy

Fedorak

Ismond²

2016

Dig Dis

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Microbiome Analytics of the Gut Microbiota in Patients With Juvenile Idiopathic Arthritis: A Longitudinal Observational Cohort Study

Dijkhuizen

Chierico

Malattia

et al. 2019

Arthritis & Rheumatology

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Objective To assess the composition of gut microbiota in Italian and Dutch patients with juvenile idiopathic arthritis ( JIA ) at baseline, with inactive disease, and with persistent activity compared to healthy controls. Methods In a multicenter, prospective, observational cohort study, fecal samples were collected at baseline from 78 Italian and 21 Dutch treatment‐naive JIA patients with <6 months of disease duration and compared to 107 geographically matched samples from healthy children. Forty‐four follow‐up samples from patients with inactive disease and 25 follow‐up samples from patients with persistent activity were analyzed. Gut microbiota composition was determined by 16S ribosomal RNA –based metagenomics. Alpha‐ and β‐diversity were computed, and log ratios of relative abundance were compared between patients and healthy controls using random forest models and logistic regression. Results Baseline samples from Italian patients showed reduced richness compared to healthy controls ( P < 0.001). Random forest models distinguished between Italian patient baseline samples and healthy controls and suggested differences between Dutch patient samples and healthy controls (areas under the curve >0.99 and 0.71, respectively). The operational taxonomic units ( OTU s) of Erysipelotrichaceae (increased in patients) , Allobaculum (decreased in patients), and Faecalibacterium prausnitzii (increased in patients) showed different relative abundance in Italian patient baseline samples compared to controls after controlling for multiple comparisons. Some OTU s differed between Dutch patient samples and healthy controls, but no evidence remained after controlling for multiple comparisons. No differences were found in paired analysis between Italian patient baseline and inactive disease samples. Conclusion Our findings show evidence for dysbiosis in JIA patients. Only patient/control status, age, and geographic origin appear to be drivers of the microbiota profiles, regardless of disease activity stage, inflammation, and markers of autoimmunity.

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mTOR inhibitor INK128 attenuates dextran sodium sulfate‐induced colitis by promotion of MDSCs on Treg cell expansion

Shi

Ren

et al. 2018

Journal Cellular Physiology

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Accumulating evidence has shown that mammalian target of rapamycin (mTOR) pathway and myeloid-derived suppressor cells (MDSCs) are involved in pathogenesis of inflammatory bowel diseases (IBDs). INK128 is a novel mTOR kinase inhibitor in clinical development. However, the exact roles of MDSCs and INK128 in IBD are unclear. Here, we showed that the INK128 treatment enhanced the resistance of mice to dextran sodium sulfate (DSS)-induced colitis and inhibited the differentiation of MDSCs into macrophages. Moreover, interferon (IFN)-α level was elevated in INK128-treated colitis mice. When stimulated with IFN-α in vitro, MDSCs showed a superior immunosuppression activity. Of note, the regulatory T cells (Tregs) increased but Th1 cells decreased in INK128-treated colitis mice. These results indicate that mTOR inhibitor INK128 attenuates DSS-induced colitis via Treg expansion promoted by MDSCs. Our work provides a new evidence that INK128 is potential to be a therapeutic drug on DSS-induced colitis via regulating MDSCs as well as maintaining Treg expansion.

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Perturbation of the Human Microbiome as a Contributor to Inflammatory Bowel Disease

Cited by 30 publications

References 109 publications

Practical Considerations and the Intestinal Microbiome in Disease: Antibiotics for IBD Therapy

Practical Considerations and the Intestinal Microbiome in Disease: Antibiotics for IBD Therapy

Microbiome Analytics of the Gut Microbiota in Patients With Juvenile Idiopathic Arthritis: A Longitudinal Observational Cohort Study

mTOR inhibitor INK128 attenuates dextran sodium sulfate‐induced colitis by promotion of MDSCs on Treg cell expansion

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