Fecal transplantation does not transfer either susceptibility or resistance to food borne listeriosis in C57BL/6 and BALB/c/By mice

Myers-Morales, Tanya; Bussell, Kate M.; D’Orazio, Sarah E. F.

doi:10.12688/f1000research.2-177.v1

Cited by 16 publications

(18 citation statements)

References 24 publications

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“…The endogenous microbiota of 12-week-old homozygous fat-1 transgenic and WT mice were depleted by treatment with a single dose of streptomycin (Sigma-Aldrich, St. Louis, MO). This process has previously been validated for fecal microbiota transplantation in conventional mice (25). It can transiently reduce by 90% the density of cecal bacteria recovered using anaerobic culture conditions and is known to return to normal levels within 3-4 days (26).…”

Section: Fecal Microbiota Transplantationmentioning

confidence: 99%

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The Transplantation of ω3 PUFA–Altered Gut Microbiota of fat-1 Mice to Wild-Type Littermates Prevents Obesity and Associated Metabolic Disorders

et al. 2018

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Altering the gut microbiome may be beneficial to the host and recently arose as a promising strategy to manage obesity. Here, we investigated the relative contribution of ω3 polyunsaturated fatty acid (PUFA)-mediated alterations in the microbiota to metabolic parameter changes in mice. Four groups were compared: male fat-1 transgenic mice (with constitutive production of ω3 PUFAs) and male wild-type (WT) littermates fed an obesogenic (high fat/high sucrose [HFHS]) or a control diet. Unlike WT mice, HFHS-fed fat-1 mice were protected against obesity, glucose intolerance, and hepatic steatosis. Unlike WT mice, fat-1 mice maintained a normal barrier function, resulting in a significantly lower metabolic endotoxemia. The fat-1 mice displayed greater phylogenic diversity in the cecum, and fecal microbiota transplantation from fat-1 to WT mice was able to reverse weight gain and to normalize glucose tolerance and intestinal permeability. We concluded that the ω3 PUFA-mediated alteration of gut microbiota contributed to the prevention of metabolic syndrome in fat-1 mice. It occurred independently of changes in the PUFA content of host tissues and may represent a promising strategy to prevent metabolic disease and preserve a lean phenotype.

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Section: Fecal Microbiota Transplantationmentioning

confidence: 99%

“…Before each fecal transfer treatment, 1 g fecal pellets were collected from eight naïve donor mice, pooled, and placed in 5 mL Dulbecco's PBS (Life Technologies, Grand Island, NY). The fecal transplantation was performed as described previously (25).…”

Section: Fecal Microbiota Transplantationmentioning

confidence: 99%

The Transplantation of ω3 PUFA–Altered Gut Microbiota of fat-1 Mice to Wild-Type Littermates Prevents Obesity and Associated Metabolic Disorders

et al. 2018

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“…To that end, we performed fecal transfer experiments as shown in Fig. A, using modified versions of milder forms of antibiotic treatments as to not completely deplete the normal mouse microbiome, which has been shown to be essential to the development of murine EAE . The data demonstrated that naïve C57BL/6mice (CD44WT) immunized with MOG and treated with streptomycin and ampicillin, followed by fecal transfer from naïve CD44KO mice showed a significant decrease in EAE clinical scores when compared to similar mice given feces from naïve CD44WT mice (Fig.…”

Section: Resultsmentioning

confidence: 99%

CD44 deletion leading to attenuation of experimental autoimmune encephalomyelitis results from alterations in gut microbiome in mice

et al. 2017

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Dysbiosis in gut microbiome has been shown to be associated with inflammatory and autoimmune diseases. Previous studies from our laboratory demonstrated the pivotal role played by CD44 in the regulation of experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis (MS). Specifically, we showed that CD44 knockout (KO) mice were resistant to induction of EAE when compared to CD44wildtype (WT) mice and this was due to inhibition in the pro-inflammatory Th1/Th17 cells and increased induction of anti-inflammatory Th2/Treg cells. In the current study, we determined whether these effects resulted from an alteration in gut microbiota and the short-chain fatty acid (SCFA) production in CD44KO mice. Fecal transfer from naïve CD44KO but not CD44WT mice, into EAE-induced CD44WT mice, led to significant amelioration of EAE. High-throughput bacterial 16S rRNA gene sequencing, followed by clustering sequences into operational taxonomic units (OTUs) and biochemical analysis, revealed that EAE-induced CD44KO mice showed significant diversity, richness, and evenness when compared to EAE-induced CD44WT mice at the phylum level, with dominant Bacteroidetes (68.5%) and low Firmicutes (26.8%). Further, data showed a significant change in the abundance of SCFAs, propionic acid and i-butyric acid in EAE-CD44KO compared to EAE-CD44WT mice. In conclusion, our results demonstrate that the attenuation of EAE seen following CD44 gene deletion in mice may result from alterations in the gut microbiota and SCFAs. Furthermore, our studies also demonstrate that the phenotype of gene knock-out animals may be shaped by gut microbiota.

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“…During feces transfer experiments, fresh stool pellets from DCA‐treated and ‐untreated mice followed by 2‐weeks' washout of DCA were suspended in reduced PBS (0.1 g/1 mL), homogenized, centrifuged at 800 g for 5 min and the supernatant was collected. Three hundred μL of supernatant was transplanted to 4‐week‐old Apc min/+ mice, which were given a gavage of streptomycin (20 mg) daily for 3 days before FMT to deplete the native gut microbiota as previously described . During transfer experiments, the mice were inoculated for a total of 16 times over the subsequent 8 weeks.…”

Section: Methodsmentioning

confidence: 99%

“…Three hundred lL of supernatant was transplanted to 4-week-old Apc min/1 mice, which were given a gavage of streptomycin (20 mg) daily for 3 days before FMT to deplete the native gut microbiota as previously described. 23,24 During transfer experiments, the mice were inoculated for a total of 16 times over the subsequent 8 weeks.…”

Section: Fecal Microbiota Transplantation (Fmt)mentioning

confidence: 99%

Secondary bile acid-induced dysbiosis promotes intestinal carcinogenesis

et al. 2017

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The gut microbiota plays an important role in maintaining intestinal homeostasis. Dysbiosis is associated with intestinal tumorigenesis. Deoxycholic acid (DCA), a secondary bile acid increased by a western diet, correlates with intestinal carcinogenesis. However, evidence relating bile acids, intestinal microbiota and tumorigenesis are limited. In our study, we investigated the effect of DCA on induction of intestinal dysbiosis and its roles in intestinal carcinogenesis. Alteration of the composition of the intestinal microbiota was induced in DCA-treated APC mice, which was accompanied by impaired intestinal barrier, gut low grade inflammation and tumor progression. The transfer of fecal microbiota from DCA-treated mice to another group of Apc mice increased tumor multiplicity, induced inflammation and recruited M2 phenotype tumor-associated macrophages. Importantly, the fecal microbiota transplantation activated the tumor-associated Wnt/β-catenin signaling pathway. Moreover, microbiota depletion by a cocktail of antibiotics was sufficient to block DCA-induced intestinal carcinogenesis, further suggesting the role of dysbiosis in tumor development. Our study demonstrated that alteration of the microbial community induced by DCA promoted intestinal carcinogenesis.

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Fecal transplantation does not transfer either susceptibility or resistance to food borne listeriosis in C57BL/6 and BALB/c/By mice

Cited by 16 publications

References 24 publications

The Transplantation of ω3 PUFA–Altered Gut Microbiota of fat-1 Mice to Wild-Type Littermates Prevents Obesity and Associated Metabolic Disorders

The Transplantation of ω3 PUFA–Altered Gut Microbiota of fat-1 Mice to Wild-Type Littermates Prevents Obesity and Associated Metabolic Disorders

CD44 deletion leading to attenuation of experimental autoimmune encephalomyelitis results from alterations in gut microbiome in mice

Secondary bile acid-induced dysbiosis promotes intestinal carcinogenesis

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