Project description:Human breast milk contains a diverse community of bacteria but factors that produce variation in the breast milk microbiome are largely unknown. We evaluated if 1) maternal factors including breastfeeding practices modified the diversity and abundance of bacterial communities in breast milk and 2) if subclinical mastitis (SCM), an asymptomatic inflammatory condition occurring during lactation, induced a distinctive microbiota signature.
| EGAS00001003044 | EGA
Project description:Human milk microbiota : total milk microbiota and cultivable milk microbiota
Project description:The factors that govern the retention and abundance of specific microbial lineages within a developing intestinal microbiota remain poorly defined. Human milk oligosaccharides consumed by nursing infnats pass undigested to the distal gut where they may be consumed by microbes. We investigated the transcriptional response of Bacterides fragilis, a prominent gut resident, to the presence of HMOs. In vitro transcriptional profiles of Bacteroides fragilis obtained from biological duplicate cultures taken at middle log phase in minimal media glucose (MM-Glu) and in minimal media with human milk oligosaccharides (MM-HMO).
Project description:The breast milk plays a crucial role in shaping the initial intestinal microbiota and mucosal immunity of the infant. Interestingly, breastfeeding has proven to be protective against the early onset of immune-mediated diseases including type 1 diabetes (T1D). Studies have shown that exosomes from human breast milk (HM) are enriched in immune-modulating miRNAs suggesting that exosomal miRNAs transferred to the infant could play a critical role in the development of the infant’s immune system. In this study, we extracted exosome exosomal microRNAs (exomiRs) from breast milk of type 1 diabetic and healthy lactating mothers, in order to identify any differences in the exomiR content between the two groups
Project description:Understanding how the human gut microbiota and host are impacted by probiotic bacterial strains requires carefully controlled studies in humans, and in mouse models of the gut ecosystem where potentially confounding variables that are difficult to control in humans can be constrained. Therefore, we characterized the fecal microbiomes and metatranscriptomes of adult female monozygotic twin pairs through repeated sampling 4 weeks prior to, 7 weeks during, and 4 weeks following consumption of a commercially-available fermented milk product (FMP) containing a consortium of Bifidobacterium animalis subsp. lactis, two strains of Lactobacillus delbrueckii subsp. bulgaricus, Lactococcus lactis subsp. cremoris, and Streptococcus thermophilus. In addition, gnotobiotic mice harboring a 15-species model human gut microbiota whose genomes contain 58,399 known or predicted protein-coding genes were studied prior to and after gavage with all five sequenced FMP strains. 140 samples total. Evaluation of changes in a model community's structure over time after exposure to a consortium of 5 fermented milk product (FMP) strains.
Project description:With this study, we wanted to investigate degradation of human milk oligosaccharides and the subsequent cross-feeding interactions of a complex bacterial community that resembles the gut microbiota of pre-weaned vaginally-born breastfed infants.
Project description:The factors that govern the retention and abundance of specific microbial lineages within a developing intestinal microbiota remain poorly defined. Human milk oligosaccharides consumed by nursing infnats pass undigested to the distal gut where they may be consumed by microbes. We investigated the transcriptional response of Bacterides fragilis, a prominent gut resident, to the presence of HMOs.
Project description:Understanding how the human gut microbiota and host are impacted by probiotic bacterial strains requires carefully controlled studies in humans, and in mouse models of the gut ecosystem where potentially confounding variables that are difficult to control in humans can be constrained. Therefore, we characterized the fecal microbiomes and metatranscriptomes of adult female monozygotic twin pairs through repeated sampling 4 weeks prior to, 7 weeks during, and 4 weeks following consumption of a commercially-available fermented milk product (FMP) containing a consortium of Bifidobacterium animalis subsp. lactis, two strains of Lactobacillus delbrueckii subsp. bulgaricus, Lactococcus lactis subsp. cremoris, and Streptococcus thermophilus. In addition, gnotobiotic mice harboring a 15-species model human gut microbiota whose genomes contain 58,399 known or predicted protein-coding genes were studied prior to and after gavage with all five sequenced FMP strains. 73 samples total. Evaluation of changes in a model community's metatranscriptome over time after exposure to a consortium of 5 fermented milk product (FMP) strains (40 samples); evaluation of the gene expression of the FMP strains in other in vitro conditions, including MRS medium (B. animalis subsp. lactis only, 4 samples) and a commercial FMP fermentation (all 5 strains, 6 samples); evaluation of the gene expression of native human microbiomes before and after the consumption of a commercial FMP (23 samples).
Project description:Breast milk is associated with multiple benefits for the infant, including reduced incidence of chronic diseases such as Inflammatory Bowel Disease. We investigated the role of milk-derived maternal IgA (matIgA) on the developing small intestinal immune system. Using a model, where genotypically identical pups were fed by dams differed only in IgA production we revealed that matIgA regulates the assembly of the infant small intestinal microbiota and epithelium, supporting Lactobacillaceae and suppressing Enterobacteriaceae and the development of secretory lineage cells. Via the microbiota, MatIgA also regulated infant immune cells and suppressed early activation of Th17 cells. We demonstrated that Enterobacteriaceae-specific CD4+ T cells, activated in the absence of matIgA, persisted long term where they may contribute to subsequent inflammatory episodes. This work suggests that maternal IgA shapes the mucosal immune response by regulating the early-life microbiota thus preventing the development of inflammatory microbiota-specific T cells with memory potential.