Abstract
BackgroundCurrent research has led to the appreciation that there are differences in the commensal microbiota between healthy individuals and individuals that are predisposed to disease. Treatments to reverse disease pathogenesis through the manipulation of the gastrointestinal (GI) microbiota are now being explored. Normalizing microbiota between different strains of mice in the same study is also needed to better understand disease pathogenesis. Current approaches require repeated delivery of bacteria and large numbers of animals and vary in treatment start time. A method is needed that can shift the microbiota of predisposed individuals to a healthy microbiota at an early age and sustain this shift through the lifetime of the individual.ResultsWe tested cross-fostering of pups within 48 h of birth as a means to permanently shift the microbiota from birth. Taxonomical analysis revealed that the nursing mother was the critical factor in determining bacterial colonization, instead of the birth mother. Data was evaluated using bacterial 16S rDNA sequences from fecal pellets and sequencing was performed on an Illumina Miseq using a 251 bp paired-end library.ConclusionsThe results show that cross-fostering is an effective means to induce an early and maintained shift in the commensal microbiota. This will allow for the evaluation of a prolonged microbial shift and its effects on disease pathogenesis. Cross-fostering will also eliminate variation within control models by normalizing the commensal microbiota between different strains of mice.Electronic supplementary materialThe online version of this article (doi:10.1186/s40168-015-0080-y) contains supplementary material, which is available to authorized users.
Highlights
Current research has led to the appreciation that there are differences in the commensal microbiota between healthy individuals and individuals that are predisposed to disease
Not birth mother, determines fecal microbiota composition The relationships between microbial communities in non-obese diabetic (NOD) and non-obese diabetic-resistant (NOR) mice that had been nursed by either NOD or NOR mothers were visualized by phylogenetic analysis using principal component of analysis (PCoA) plots using the unweighted unifrac distance matrices (Figure 2)
Feces from 4-week-old NOD and NOR pups nursed by a NOR mother have microbiota resembling that of NOR mice, while feces from 4-week-old NOD and NOR mice nursed by a NOD mother have microbiota resembling that of NOD mice
Summary
Current research has led to the appreciation that there are differences in the commensal microbiota between healthy individuals and individuals that are predisposed to disease. A method is needed that can shift the microbiota of predisposed individuals to a healthy microbiota at an early age and sustain this shift through the lifetime of the individual In recent years, it has been appreciated in both animal models and human patients that there are healthy and disease-promoting microbiota [1,2,3]. In order to study the effects of the microbiota in healthy and diseased subjects, research has focused on replacing or shifting disease-promoting microbiota to healthy microbiota, potentially reversing the diseased state. Experiments with toll-like receptor (TLR) knockouts and wild-type mice born to TLR knockout mothers via a heterozygous breeding reveal an identical microbiota between all pups regardless of TLR status [18].
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