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- Livanos, A. E., et al.
(author)
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Antibiotic-mediated gut microbiome perturbation accelerates development of type 1 diabetes in mice
- 2016
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In: Nature Microbiology. - : Springer Science and Business Media LLC. - 2058-5276. ; 1
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Journal article (peer-reviewed)abstract
- The early life microbiome plays important roles in host immunological and metabolic development. Because the incidence of type 1 diabetes (T1D) has been increasing substantially in recent decades, we hypothesized that early-life antibiotic use alters gut microbiota, which predisposes to disease. Using non-obese diabetic mice that are genetically susceptible to T1D, we examined the effects of exposure to either continuous low-dose antibiotics or pulsed therapeutic antibiotics (PAT) early in life, mimicking childhood exposures. We found that in mice receiving PAT, T1D incidence was significantly higher, and microbial community composition and structure differed compared with controls. In pre-diabetic male PAT mice, the intestinal lamina propria had lower Th17 and T reg proportions and intestinal SAA expression than in controls, suggesting key roles in transducing the altered microbiota signals. PAT affected microbial lipid metabolism and host cholesterol biosynthetic gene expression. These findings show that early-life antibiotic treatments alter the gut microbiota and its metabolic capacities, intestinal gene expression and T-cell populations, accelerating T1D onset in non-obese diabetic mice.
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| 4. |
- Zhang, X. S., et al.
(author)
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Maternal cecal microbiota transfer rescues early-life antibiotic-induced enhancement of type 1 diabetes in mice
- 2021
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In: Cell Host & Microbe. - : Elsevier BV. - 1931-3128. ; 29:8
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Journal article (peer-reviewed)abstract
- Early-life antibiotic exposure perturbs the intestinal microbiota and accelerates type 1 diabetes (T1D) development in the NOD mouse model. Here, we found that maternal cecal m icrobiota transfer (CMT) to NOD mice after early-life antibiotic perturbation largely rescued the induced T1D enhancement. Restoration of the intestinal microbiome was significant and persistent, remediating the antibiotic-depleted diversity, relative abundance of particular taxa, and metabolic pathways. CMT also protected against perturbed metabolites and normalized innate and adaptive immune effectors. CMT restored major patterns of ileal microRNA and histone regulation of gene expression. Further experiments suggest a gut-microbiota-regulated T1D protection mechanism centered on Reg3 gamma, in an innate intestinal immune network involving CD44, TLR2, and Reg3 gamma. This regulation affects downstream immunological tone, which may lead to protection against tissue-specific T1D injury.
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- Costea, P. I., et al.
(author)
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Enterotypes in the landscape of gut microbial community composition
- 2018
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In: Nature Microbiology. - : Springer Science and Business Media LLC. - 2058-5276. ; 3:1
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Journal article (peer-reviewed)abstract
- Population stratification is a useful approach for a better understanding of complex biological problems in human health and wellbeing. The proposal that such stratification applies to the human gut microbiome, in the form of distinct community composition types termed enterotypes, has been met with both excitement and controversy. In view of accumulated data and re-analyses since the original work, we revisit the concept of enterotypes, discuss different methods of dividing up the landscape of possible microbiome configurations, and put these concepts into functional, ecological and medical contexts. As enterotypes are of use in describing the gut microbial community landscape and may become relevant in clinical practice, we aim to reconcile differing views and encourage a balanced application of the concept.
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- Lahiri, S, et al.
(author)
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The gut microbiota influences skeletal muscle mass and function in mice
- 2019
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In: Science translational medicine. - : American Association for the Advancement of Science (AAAS). - 1946-6242 .- 1946-6234. ; 11:502
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Journal article (peer-reviewed)abstract
- Transplanting the gut microbiota of pathogen-free mice into germ-free mice improves skeletal muscle mass and strength.
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| 10. |
- Munoz-Ramirez, Z. Y., et al.
(author)
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A 500-year tale of co-evolution, adaptation, and virulence:Helicobacter pyloriin the Americas
- 2021
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In: Isme Journal. - : Springer Science and Business Media LLC. - 1751-7362 .- 1751-7370. ; 15:1, s. 78-92
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Journal article (peer-reviewed)abstract
- Helicobacter pyloriis a common component of the human stomach microbiota, possibly dating back to the speciation ofHomo sapiens. A history of pathogen evolution in allopatry has led to the development of genetically distinctH. pylorisubpopulations, associated with different human populations, and more recent admixture amongH. pylorisubpopulations can provide information about human migrations. However, little is known about the degree to which someH. pylorigenes are conserved in the face of admixture, potentially indicating host adaptation, or how virulence genes spread among different populations. We analyzedH. pylorigenomes from 14 countries in the Americas, strains from the Iberian Peninsula, and public genomes from Europe, Africa, and Asia, to investigate how admixture varies across different regions and gene families. Whole-genome analyses of 723H. pyloristrains from around the world showed evidence of frequent admixture in the American strains with a complex mosaic of contributions fromH. pyloripopulations originating in the Americas as well as other continents. Despite the complex admixture, distinctive genomic fingerprints were identified for each region, revealing novel AmericanH. pylorisubpopulations. A pan-genome Fst analysis showed that variation in virulence genes had the strongest fixation in America, compared with non-American populations, and that much of the variation constituted non-synonymous substitutions in functional domains. Network analyses suggest that these virulence genes have followed unique evolutionary paths in the American populations, spreading into different genetic backgrounds, potentially contributing to the high risk of gastric cancer in the region.
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