Dynamic and Asymmetric Changes of the Microbial Communities after Cohousing in Laboratory Mice

Caruso, Roberta; Ono, Masahiro; Bunker, Marie; Núñez, Gabriel; Inohara, Naohiro

doi:10.1016/j.celrep.2019.05.042

Cited by 82 publications

(89 citation statements)

References 52 publications

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“…As described above, cohousing transfers gut microbiota from one mouse to its cagemates and normalizes differences in their gut microbiota [18,19]. For this reason, cohousing has been used as a means to evaluate effects of the gut microbiome on physiological endpoints.…”

Section: Effect Of Cohousing On Hfd-and St2-dependent Changes In Pulmmentioning

confidence: 99%

“…We have recently reported a role for the microbiome in the effects of ST2 deficiency on O 3 -induced AHR in lean male mice: compared to WT mice, ST2 deficient mice housed with other ST2-deficient mice (same housed mice) have reduced O 3 -induced AHR, but housing ST2 deficient mice with WT mice (cohousing) reverts the magnitude of their O 3 -induced to that observed in WT mice [17]. Because mice ingest some of the fecal microbiota of their cagemates either during grooming or as a result of coprophagy, cohousing transfers gut microbiota from one mouse to its cagemates and rapidly normalizes differences in their gut microbiota [18,19]. Indeed, we observed effects of both ST2 deficiency and effects of cohousing on the gut microbial community structures of these lean chow-fed mice [17].…”

Section: Introductionmentioning

confidence: 99%

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IL-33, diet-induced obesity, and pulmonary responses to ozone

Kasahara¹,

Shore²

2020

Respir Res

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Background: Obesity augments pulmonary responses to ozone. We have reported that IL-33 contributes to these effects of obesity in db/db mice. The purpose of this study was to determine whether IL-33 also contributes to obesity-related changes in the response to ozone in mice with diet-induced obesity. Methods: Male wildtype C57BL/6 mice and mice deficient in ST2, the IL-33 receptor, were placed on chow or high fat diets for 12 weeks from weaning. Because the microbiome has been implicated in obesity-related changes in the pulmonary response to ozone, mice were either housed with other mice of the same genotype (same housed) or with mice of the opposite genotype (cohoused). Cohousing transfers the gut microbiome from one mouse to its cagemates. Results: Diet-induced increases in body mass were not affected by ST2 deficiency or cohousing. In same housed mice, ST2 deficiency reduced ozone-induced airway hyperresponsiveness and neutrophil recruitment in chow-fed but not HFDfed mice even though ST2 deficiency reduced bronchoalveolar lavage IL-5 in both diet groups. In chow-fed mice, cohousing abolished ST2-related reductions in ozone-induced airway hyperresponsiveness and neutrophil recruitment, but in HFD-fed mice, no effect of cohousing on these responses to ozone was observed. In chow-fed mice, ST2 deficiency and cohousing caused changes in the gut microbiome. High fat diet-feeding caused marked changes in the gut microbiome and overrode both ST2-related and cohousing-related differences in the gut microbiome observed in chow-fed mice. Conclusion: Our data indicate a role for IL-33 in pulmonary responses to ozone in chow-fed but not high fat diet-fed mice and are consistent with the hypothesis that these diet-related differences in the role of IL-33 are the result of changes in the gut microbiome.

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Section: Effect Of Cohousing On Hfd-and St2-dependent Changes In Pulmmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

IL-33, diet-induced obesity, and pulmonary responses to ozone

Kasahara¹,

Shore²

2020

Respir Res

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“…Microbiota composition was determined by sequencing the V4 region of the 16S rRNA gene (≈250 bp) from the 5′ and 3′ ends with Illumina MiSeq and the resulting reads were assembled and analyzed by Mothur, as described previously. 15 The OTUs were classified into taxonomic phylotypes at >97% identity. The Shannon, Chao, and Simpson diversity indexes, Shannon evenness index, θ YC , and Bray-Curtis dissimilarity indexes were calculated by Mothur, whereas the operational taxonomic unit (OTU) richness was calculated by Microsoft Excel.…”

Section: Microbiota Analysismentioning

confidence: 99%

Impact of dietary manganese on experimental colitis in mice

et al. 2019

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Diet plays a significant role in the pathogenesis of inflammatory bowel disease (IBD). A recent epidemiological study has shown an inverse relationship between nutritional manganese (Mn) status and IBD patients. Mn is an essential micronutrient required for normal cell function and physiological processes. To date, the roles of Mn in intestinal homeostasis remain unknown and the contribution of Mn to IBD has yet to be explored. Here, we provide evidence that Mn is critical for the maintenance of the intestinal barrier and that Mn deficiency exacerbates dextran sulfate sodium (DSS)-induced colitis in mice. Specifically, when treated with DSS, Mn-deficient mice showed increased morbidity, weight loss, and colon injury, with a concomitant increase in inflammatory cytokine levels and oxidative and DNA damage. Even without DSS treatment, dietary Mn deficiency alone increased intestinal permeability by impairing intestinal tight junctions. In contrast, mice fed a Mn-supplemented diet showed slightly increased tolerance to DSS-induced experimental colitis, as judged by the colon length. Despite the well-appreciated roles of intestinal microbiota in driving inflammation in IBD, the gut microbiome composition was not altered by changes in dietary Mn. We conclude that Mn is necessary for proper maintenance of the intestinal barrier and provides protection against DSS-induced colon injury. K E Y W O R D Scolitis, gut microbiota, inflammatory bowel disease, manganese, tight junction 2930 | CHOI et al. | RNA isolation and RT-PCR

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“…Next, to investigate whether horizontal transmission of the microbiota during adulthood might account for Th17 expansion, WT and LXRα −/− non-littermate mice from the same provider were either co-housed or single housed according to their genotype for 4 weeks ( Fig. 4c ) to allow for normalization of microbiota 18 . Of note, WT mice co-housed with LXRα −/− mice partially gained higher frequencies of MLN Th17 cells compared to single housed WT mice.…”

Section: Resultsmentioning

confidence: 99%

Liver X Receptor regulates Th17 and RORγt⁺ Treg cells by distinct mechanisms

Parigi

Das

Frede

et al. 2019

Preprint

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22The gastrointestinal microenvironment, dominated by dietary compounds and the commensal bacteria, 23 is a major driver of intestinal CD4 + T helper (Th) cell differentiation. Dietary compounds can be sensed 24 by nuclear receptors (NRs) that consequently exerts pleiotropic effects including immune modulation. 25However, how NRs regulate distinct intestinal Th subsets remain poorly understood. Here, we found 26 that under homeostatic condition Liver X receptor (LXR), a sensor of cholesterol metabolites, controls 27RORγt + Treg and Th17 cells in the intestine draining mesenteric lymph node (MLN). Mechanistically, 28 while lack of LXR signaling in CD11c + myeloid cells led to an increase in RORγt + Treg, modulation 29 of MLN Th17 was independent of LXR signaling in either immune or epithelial cells. Of note, LXRα 30 modulated only the Th17 cells, but not RORγt + Treg in the MLN and horizontal transfer of microbiota 31 between LXRα −/− and WT mice was sufficient to partially increase the MLN Th17 in WT mice. While 32LXRα deficiency increased the abundance of Ruminococcaceae and Lachnospiraceae bacterial 33 families compared to the WT littermates, microbiota ablation including ablation of SFB was not 34 sufficient to dampen LXRα-mediated expansion of MLN Th17. Altogether, our results suggest that 35 LXR modulates RORγt + Treg and Th17 cells in the MLN through distinct mechanisms.The intestinal barrier is continuously exposed to the changing external environment. To face this 56 challenge, our immune system has evolved to rapidly adapt to environmental changes by mounting 57 tolerogenic and effector responses on demand. A dynamic equilibrium between these two arms of the 58 immune system is required to maintain homeostasis, and failure of mounting an appropriate regulatory 59 response may lead to uncontrolled inflammatory reactions and chronic immune disorders. 60Owing to their ability to react in an antigen-specific manner CD4 + T helper (Th) cells are central 61 players in ensuring a protective response while limiting collateral damage. Mounting a functional Th 62 cell response in the intestine relies on the anatomical distribution of T cells in immunological inductive 63 and effector sites, where the former is constituted by intestine-draining lymphoid structures such as 64 MLN and the latter being the intraepithelial and lamina propria compartments 1 . The inductive sites 65 represent the arena where naïve CD4 + T cells encounter their cognate antigens for the first time and 66 functionally commit to specific effector subsets. Under steady state, retinoic acid-related orphan 67 receptor gt (RORgt) + Th cells (Th17) and Foxp3 expressing regulatory T cells (Treg) are the most 68 represented Th subsets in the MLN. Despite a certain degree of lineage and functional flexibility, Th17 69 and Treg cells play complementary roles in maintaining intestinal homeostasis. Although the 70 expression of RORgt and Foxp3 was originally thought to be mutually exclusive, a distinct new 71 population of RORgt + Foxp3 + regulatory T ...

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Dynamic and Asymmetric Changes of the Microbial Communities after Cohousing in Laboratory Mice

Cited by 82 publications

References 52 publications

IL-33, diet-induced obesity, and pulmonary responses to ozone

IL-33, diet-induced obesity, and pulmonary responses to ozone

Impact of dietary manganese on experimental colitis in mice

Liver X Receptor regulates Th17 and RORγt⁺ Treg cells by distinct mechanisms

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Dynamic and Asymmetric Changes of the Microbial Communities after Cohousing in Laboratory Mice

Cited by 82 publications

References 52 publications

IL-33, diet-induced obesity, and pulmonary responses to ozone

IL-33, diet-induced obesity, and pulmonary responses to ozone

Impact of dietary manganese on experimental colitis in mice

Liver X Receptor regulates Th17 and RORγt+ Treg cells by distinct mechanisms

Contact Info

Product

Resources

About

Liver X Receptor regulates Th17 and RORγt⁺ Treg cells by distinct mechanisms